CIDeRplusGeneral Information:
| Id: | 8,153 |
| Diseases: |
Diabetes mellitus, type II
- [OMIM]
Insulin resistance |
| Mammalia | |
| review | |
| Reference: | Gooding JR et al.(2016) Metabolomics applied to the pancreatic islet Arch. Biochem. Biophys. 589: 120-130 [PMID: 26116790] |
Interaction Information:
| Comment | The contributions of glycogen synthesis and the pentose phosphate pathway (PPP) to total glucose utilization are thought to be low in beta-cells, and more than 90% of glucose molecules entering beta-cells are estimated to engage in glycolysis and subsequent mitochondrial metabolism. |
|
Formal Description Interaction-ID: 81757 |
process affects_activity of process glucose utilization |
| Comment | The contributions of glycogen synthesis and the pentose phosphate pathway (PPP) to total glucose utilization are thought to be low in beta-cells, and more than 90% of glucose molecules entering beta-cells are estimated to engage in glycolysis and subsequent mitochondrial metabolism. |
|
Formal Description Interaction-ID: 81948 |
process affects_activity of process glucose utilization |
| Comment | The contributions of glycogen synthesis and the pentose phosphate pathway (PPP) to total glucose utilization are thought to be low in beta-cells, and more than 90% of glucose molecules entering beta-cells are estimated to engage in glycolysis and subsequent mitochondrial metabolism. |
|
Formal Description Interaction-ID: 81949 |
process affects_activity of process glucose utilization |
| Comment | Unbiased metabolomics analysis of 832/13 cells has demonstrated a significant glucose-induced increment of all glycolytic intermediates measured (glucose 6-phosphate, fructose 1,6-bisphosphate, dihydroxyactone phosphate, 2/3-phosphoglycerate, phosphoenolpyruvate and pyruvate). Furthermore, targeted as well as unbiased metabolomics analyses have revealed a robust increase in TCA intermediates ((iso)citrate, aconitate, alpha-ketoglutarate, succinate, fumarate and malate) in response to 45‚Äď120 min of glucose stimulation. |
|
Formal Description Interaction-ID: 81950 |
process glucose utilization increases_quantity of drug/chemical compound |
| Comment | Unbiased metabolomics analysis of 832/13 cells has demonstrated a significant glucose-induced increment of all glycolytic intermediates measured (glucose 6-phosphate, fructose 1,6-bisphosphate, dihydroxyacetone phosphate, 2/3-phosphoglycerate, phosphoenolpyruvate and pyruvate). Furthermore, targeted as well as unbiased metabolomics analyses have revealed a robust increase in TCA intermediates ((iso)citrate, aconitate, alpha-ketoglutarate, succinate, fumarate and malate) in response to 45‚Äď120 min of glucose stimulation. |
|
Formal Description Interaction-ID: 81951 |
process glucose utilization increases_quantity of drug/chemical compound |
| Comment | Unbiased metabolomics analysis of 832/13 cells has demonstrated a significant glucose-induced increment of all glycolytic intermediates measured (glucose 6-phosphate, fructose 1,6-bisphosphate, dihydroxyacetone phosphate, 2/3-phosphoglycerate, phosphoenolpyruvate and pyruvate). Furthermore, targeted as well as unbiased metabolomics analyses have revealed a robust increase in TCA intermediates ((iso)citrate, aconitate, alpha-ketoglutarate, succinate, fumarate and malate) in response to 45‚Äď120 min of glucose stimulation. |
|
Formal Description Interaction-ID: 81952 |
process glucose utilization increases_quantity of drug/chemical compound |
| Comment | Unbiased metabolomics analysis of 832/13 cells has demonstrated a significant glucose-induced increment of all glycolytic intermediates measured (glucose 6-phosphate, fructose 1,6-bisphosphate, dihydroxyacetone phosphate, 2/3-phosphoglycerate, phosphoenolpyruvate and pyruvate). Furthermore, targeted as well as unbiased metabolomics analyses have revealed a robust increase in TCA intermediates ((iso)citrate, aconitate, alpha-ketoglutarate, succinate, fumarate and malate) in response to 45‚Äď120 min of glucose stimulation. |
|
Formal Description Interaction-ID: 81953 |
process glucose utilization increases_quantity of drug/chemical compound |
| Comment | Unbiased metabolomics analysis of 832/13 cells has demonstrated a significant glucose-induced increment of all glycolytic intermediates measured (glucose 6-phosphate, fructose 1,6-bisphosphate, dihydroxyacetone phosphate, 2/3-phosphoglycerate, phosphoenolpyruvate and pyruvate). Furthermore, targeted as well as unbiased metabolomics analyses have revealed a robust increase in TCA intermediates ((iso)citrate, aconitate, alpha-ketoglutarate, succinate, fumarate and malate) in response to 45‚Äď120 min of glucose stimulation. |
|
Formal Description Interaction-ID: 81954 |
process glucose utilization increases_quantity of drug/chemical compound 2-Phosphoglycerate |
| Comment | Unbiased metabolomics analysis of 832/13 cells has demonstrated a significant glucose-induced increment of all glycolytic intermediates measured (glucose 6-phosphate, fructose 1,6-bisphosphate, dihydroxyacetone phosphate, 2/3-phosphoglycerate, phosphoenolpyruvate and pyruvate). Furthermore, targeted as well as unbiased metabolomics analyses have revealed a robust increase in TCA intermediates ((iso)citrate, aconitate, alpha-ketoglutarate, succinate, fumarate and malate) in response to 45‚Äď120 min of glucose stimulation. |
|
Formal Description Interaction-ID: 81955 |
process glucose utilization increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for |
| Comment | Unbiased metabolomics analysis of 832/13 cells has demonstrated a significant glucose-induced increment of all glycolytic intermediates measured (glucose 6-phosphate, fructose 1,6-bisphosphate, dihydroxyacetone phosphate, 2/3-phosphoglycerate, phosphoenolpyruvate and pyruvate). Furthermore, targeted as well as unbiased metabolomics analyses have revealed a robust increase in TCA intermediates ((iso)citrate, aconitate, alpha-ketoglutarate, succinate, fumarate and malate) in response to 45‚Äď120 min of glucose stimulation. |
|
Formal Description Interaction-ID: 81956 |
process glucose utilization increases_quantity of drug/chemical compound |
| Comment | Unbiased metabolomics analysis of 832/13 cells has demonstrated a significant glucose-induced increment of all glycolytic intermediates measured (glucose 6-phosphate, fructose 1,6-bisphosphate, dihydroxyacetone phosphate, 2/3-phosphoglycerate, phosphoenolpyruvate and pyruvate). Furthermore, targeted as well as unbiased metabolomics analyses have revealed a robust increase in TCA intermediates ((iso)citrate, aconitate, alpha-ketoglutarate, succinate, fumarate and malate) in response to 45‚Äď120 min of glucose stimulation. |
|
Formal Description Interaction-ID: 81957 |
process glucose utilization increases_quantity of drug/chemical compound |
| Comment | Unbiased metabolomics analysis of 832/13 cells has demonstrated a significant glucose-induced increment of all glycolytic intermediates measured (glucose 6-phosphate, fructose 1,6-bisphosphate, dihydroxyacetone phosphate, 2/3-phosphoglycerate, phosphoenolpyruvate and pyruvate). Furthermore, targeted as well as unbiased metabolomics analyses have revealed a robust increase in TCA intermediates ((iso)citrate, aconitate, alpha-ketoglutarate, succinate, fumarate and malate) in response to 45‚Äď120 min of glucose stimulation. |
|
Formal Description Interaction-ID: 81958 |
process glucose utilization increases_quantity of drug/chemical compound |
| Comment | Unbiased metabolomics analysis of 832/13 cells has demonstrated a significant glucose-induced increment of all glycolytic intermediates measured (glucose 6-phosphate, fructose 1,6-bisphosphate, dihydroxyacetone phosphate, 2/3-phosphoglycerate, phosphoenolpyruvate and pyruvate). Furthermore, targeted as well as unbiased metabolomics analyses have revealed a robust increase in TCA intermediates ((iso)citrate, aconitate, alpha-ketoglutarate, succinate, fumarate and malate) in response to 45‚Äď120 min of glucose stimulation. |
|
Formal Description Interaction-ID: 81959 |
process glucose utilization increases_quantity of drug/chemical compound |
| Comment | Unbiased metabolomics analysis of 832/13 cells has demonstrated a significant glucose-induced increment of all glycolytic intermediates measured (glucose 6-phosphate, fructose 1,6-bisphosphate, dihydroxyacetone phosphate, 2/3-phosphoglycerate, phosphoenolpyruvate and pyruvate). Furthermore, targeted as well as unbiased metabolomics analyses have revealed a robust increase in TCA intermediates ((iso)citrate, aconitate, alpha-ketoglutarate, succinate, fumarate and malate) in response to 45‚Äď120 min of glucose stimulation. |
|
Formal Description Interaction-ID: 81960 |
process glucose utilization increases_quantity of drug/chemical compound |
| Comment | Unbiased metabolomics analysis of 832/13 cells has demonstrated a significant glucose-induced increment of all glycolytic intermediates measured (glucose 6-phosphate, fructose 1,6-bisphosphate, dihydroxyacetone phosphate, 2/3-phosphoglycerate, phosphoenolpyruvate and pyruvate). Furthermore, targeted as well as unbiased metabolomics analyses have revealed a robust increase in TCA intermediates ((iso)citrate, aconitate, alpha-ketoglutarate, succinate, fumarate and malate) in response to 45‚Äď120 min of glucose stimulation. |
|
Formal Description Interaction-ID: 81961 |
process glucose utilization increases_quantity of drug/chemical compound |
| Comment | Unbiased metabolomics analysis of 832/13 cells has demonstrated a significant glucose-induced increment of all glycolytic intermediates measured (glucose 6-phosphate, fructose 1,6-bisphosphate, dihydroxyacetone phosphate, 2/3-phosphoglycerate, phosphoenolpyruvate and pyruvate). Furthermore, targeted as well as unbiased metabolomics analyses have revealed a robust increase in TCA intermediates ((iso)citrate, aconitate, alpha-ketoglutarate, succinate, fumarate and malate) in response to 45‚Äď120 min of glucose stimulation. |
|
Formal Description Interaction-ID: 81962 |
process glucose utilization increases_quantity of drug/chemical compound |
| Comment | Unbiased metabolomics analysis of 832/13 cells has demonstrated a significant glucose-induced increment of all glycolytic intermediates measured (glucose 6-phosphate, fructose 1,6-bisphosphate, dihydroxyacetone phosphate, 2/3-phosphoglycerate, phosphoenolpyruvate and pyruvate). Furthermore, targeted as well as unbiased metabolomics analyses have revealed a robust increase in TCA intermediates ((iso)citrate, aconitate, alpha-ketoglutarate, succinate, fumarate and malate) in response to 45‚Äď120 min of glucose stimulation. |
|
Formal Description Interaction-ID: 81963 |
process glucose utilization increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for |
| Comment | Unbiased metabolomics analysis of 832/13 cells has demonstrated a significant glucose-induced increment of all glycolytic intermediates measured (glucose 6-phosphate, fructose 1,6-bisphosphate, dihydroxyacetone phosphate, 2/3-phosphoglycerate, phosphoenolpyruvate and pyruvate). Furthermore, targeted as well as unbiased metabolomics analyses have revealed a robust increase in TCA intermediates ((iso)citrate, aconitate, alpha-ketoglutarate, succinate, fumarate and malate) in response to 45‚Äď120 min of glucose stimulation. |
|
Formal Description Interaction-ID: 81964 |
process glucose utilization increases_quantity of drug/chemical compound |
| Comment | Unbiased metabolomics analysis of 832/13 cells has demonstrated a significant glucose-induced increment of all glycolytic intermediates measured (glucose 6-phosphate, fructose 1,6-bisphosphate, dihydroxyacetone phosphate, 2/3-phosphoglycerate, phosphoenolpyruvate and pyruvate). Furthermore, targeted as well as unbiased metabolomics analyses have revealed a robust increase in TCA intermediates ((iso)citrate, aconitate, alpha-ketoglutarate, succinate, fumarate and malate) in response to 45‚Äď120 min of glucose stimulation. |
|
Formal Description Interaction-ID: 81965 |
process glucose utilization increases_quantity of drug/chemical compound |
| Comment | Unbiased metabolomics analysis of 832/13 cells has demonstrated a significant glucose-induced increment of all glycolytic intermediates measured (glucose 6-phosphate, fructose 1,6-bisphosphate, dihydroxyacetone phosphate, 2/3-phosphoglycerate, phosphoenolpyruvate and pyruvate). Furthermore, targeted as well as unbiased metabolomics analyses have revealed a robust increase in TCA intermediates ((iso)citrate, aconitate, alpha-ketoglutarate, succinate, fumarate and malate) in response to 45‚Äď120 min of glucose stimulation. |
|
Formal Description Interaction-ID: 81966 |
process glucose utilization increases_quantity of drug/chemical compound |
| Comment | Several labs have explored metabolic changes during the first phase of insulin secretion using metabolomics and have detected significant increases in glycolytic and TCA intermediates within 2‚Äď15 min of glucose stimulation in 832/13 cells. |
|
Formal Description Interaction-ID: 81967 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Several labs have explored metabolic changes during the first phase of insulin secretion using metabolomics and have detected significant increases in glycolytic and TCA intermediates within 2‚Äď15 min of glucose stimulation in 832/13 cells. |
|
Formal Description Interaction-ID: 81969 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Several labs have explored metabolic changes during the first phase of insulin secretion using metabolomics and have detected significant increases in glycolytic and TCA intermediates within 2‚Äď15 min of glucose stimulation in 832/13 cells. |
|
Formal Description Interaction-ID: 81970 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Several labs have explored metabolic changes during the first phase of insulin secretion using metabolomics and have detected significant increases in glycolytic and TCA intermediates within 2‚Äď15 min of glucose stimulation in 832/13 cells. |
|
Formal Description Interaction-ID: 81971 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Several labs have explored metabolic changes during the first phase of insulin secretion using metabolomics and have detected significant increases in glycolytic and TCA intermediates within 2‚Äď15 min of glucose stimulation in 832/13 cells. |
|
Formal Description Interaction-ID: 81972 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Several labs have explored metabolic changes during the first phase of insulin secretion using metabolomics and have detected significant increases in glycolytic and TCA intermediates within 2‚Äď15 min of glucose stimulation in 832/13 cells. |
|
Formal Description Interaction-ID: 81973 |
process insulin secretion, first phase increases_quantity of drug/chemical compound 2-Phosphoglycerate |
| Comment | Several labs have explored metabolic changes during the first phase of insulin secretion using metabolomics and have detected significant increases in glycolytic and TCA intermediates within 2‚Äď15 min of glucose stimulation in 832/13 cells. |
|
Formal Description Interaction-ID: 81974 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for |
| Comment | Several labs have explored metabolic changes during the first phase of insulin secretion using metabolomics and have detected significant increases in glycolytic and TCA intermediates within 2‚Äď15 min of glucose stimulation in 832/13 cells. |
|
Formal Description Interaction-ID: 81975 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Several labs have explored metabolic changes during the first phase of insulin secretion using metabolomics and have detected significant increases in glycolytic and TCA intermediates within 2‚Äď15 min of glucose stimulation in 832/13 cells. |
|
Formal Description Interaction-ID: 81976 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Several labs have explored metabolic changes during the first phase of insulin secretion using metabolomics and have detected significant increases in glycolytic and TCA intermediates within 2‚Äď15 min of glucose stimulation in 832/13 cells. |
|
Formal Description Interaction-ID: 81977 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Several labs have explored metabolic changes during the first phase of insulin secretion using metabolomics and have detected significant increases in glycolytic and TCA intermediates within 2‚Äď15 min of glucose stimulation in 832/13 cells. |
|
Formal Description Interaction-ID: 81978 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Several labs have explored metabolic changes during the first phase of insulin secretion using metabolomics and have detected significant increases in glycolytic and TCA intermediates within 2‚Äď15 min of glucose stimulation in 832/13 cells. |
|
Formal Description Interaction-ID: 81979 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Several labs have explored metabolic changes during the first phase of insulin secretion using metabolomics and have detected significant increases in glycolytic and TCA intermediates within 2‚Äď15 min of glucose stimulation in 832/13 cells. |
|
Formal Description Interaction-ID: 81980 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Several labs have explored metabolic changes during the first phase of insulin secretion using metabolomics and have detected significant increases in glycolytic and TCA intermediates within 2‚Äď15 min of glucose stimulation in 832/13 cells. |
|
Formal Description Interaction-ID: 81981 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Several labs have explored metabolic changes during the first phase of insulin secretion using metabolomics and have detected significant increases in glycolytic and TCA intermediates within 2‚Äď15 min of glucose stimulation in 832/13 cells. |
|
Formal Description Interaction-ID: 81982 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for |
| Comment | Several labs have explored metabolic changes during the first phase of insulin secretion using metabolomics and have detected significant increases in glycolytic and TCA intermediates within 2‚Äď15 min of glucose stimulation in 832/13 cells. |
|
Formal Description Interaction-ID: 81983 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | In the first phase of insulin secretion a drop in AMP and ADP was observed, resulting in a distinct increment in ATP/ADP ratio within the first 5 min of glucose stimulation which is in agreement with an important role of K-ATP channels in triggering the first phase of insulin secretion. |
|
Formal Description Interaction-ID: 81984 |
process insulin secretion, first phase decreases_quantity of drug/chemical compound |
| Comment | In the first phase of insulin secretion a drop in AMP and ADP was observed, resulting in a distinct increment in ATP/ADP ratio within the first 5 min of glucose stimulation which is in agreement with an important role of K-ATP channels in triggering the first phase of insulin secretion. |
|
Formal Description Interaction-ID: 81985 |
process insulin secretion, first phase decreases_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 81986 |
process insulin secretion, first phase decreases_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 81987 |
process insulin secretion, first phase decreases_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 81988 |
process insulin secretion, first phase decreases_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 81989 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 81990 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 81991 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 81993 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 81994 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 81995 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 81996 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 81997 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 81998 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 81999 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 82000 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 82001 |
process insulin secretion, first phase decreases_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 82002 |
process insulin secretion, first phase decreases_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 82003 |
process insulin secretion, first phase decreases_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 82004 |
process insulin secretion, first phase decreases_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 82005 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 82008 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 82009 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 82010 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 82011 |
process insulin secretion, first phase affects_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 82013 |
process insulin secretion, first phase affects_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 82014 |
process insulin secretion, first phase affects_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 82015 |
process insulin secretion, first phase affects_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 82016 |
process insulin secretion, first phase affects_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 82017 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 82018 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 82019 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 82020 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 82021 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 82022 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 82023 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for |
| Comment | Using untargeted GC‚ÄďMS in 832/13 cells, first phase insulin secretion was also found to be negatively associated with aspartate, lysine and proline and positively with ribose-5-phosphate, 6-phosphoglucono-1,5-lactone, gulonic acid gamma-lactone, ribitol, sedoheptulose, N-acetylglucosamine, lactose, sorbitol, fructose, alanine, and 3-aminoisobutyrate. In another GC‚ÄďMS based study, first phase insulin secretion was found to be negatively correlated with aspartate, (iso)leucine, hydroxyproline, proline and valine, and positively correlated with ribose-5-phosphate, lactate, glycerol-3-phosphate, alanine, cysteine, glutamate, and glycine. Another study found an inverse relationship between asparagine, glutamine, lysine, serine, long chain fatty acids, long-chain acyl-CoAs, HMG-CoA, NADP, mono- and diphosphonucleotides and first phase insulin secretion using unbiased LC‚ÄďMS/MS in glucose-stimulated 832/13 cells. In contrast, this group also observed increases in farnesyl pyrophosphate, NADH, 6-phosphogluconate, sedoheptulose phosphate, phosphoribosyl pyrophosphate, ZMP, glycinamideribotide, and GDP-mannose. |
|
Formal Description Interaction-ID: 82025 |
process insulin secretion, first phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82026 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82029 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82030 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82031 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82032 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82033 |
process insulin secretion, second phase increases_quantity of drug/chemical compound 2-Phosphoglycerate |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82034 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82035 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82036 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82037 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82038 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82039 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82040 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82041 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82042 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82043 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82044 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82045 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82046 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82047 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82048 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82049 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82050 |
process insulin secretion, second phase affects_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82051 |
process insulin secretion, second phase affects_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82052 |
process insulin secretion, second phase affects_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82053 |
process insulin secretion, second phase affects_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82054 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82055 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82056 |
process insulin secretion, second phase decreases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82057 |
process insulin secretion, second phase affects_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82058 |
process insulin secretion, second phase decreases_quantity of drug/chemical compound BABA |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82059 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82060 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82061 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82062 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82063 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82064 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82065 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82066 |
process insulin secretion, second phase increases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82067 |
process insulin secretion, second phase decreases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82068 |
process insulin secretion, second phase decreases_quantity of drug/chemical compound |
| Comment | The second phase of insulin secretion correlates with elevated pools of glycolytic and TCA intermediates. Furthermore, the changes in nucleotide levels, PPP intermediates and long chain fatty acids observed in the first phase by unbiased LC‚ÄďMS/MS are sustained in the second phase. Also, PPP intermediates ribose 5-phophate and 6-phosphogluconate, and the amino acids alanine, (iso)leucine, lysine, serine, and medium and long chain fatty acids associate with the second phase, whereas aspartate, sarcosine, and 3-aminobutyric acid are down-regulated by glucose (unbiased GC‚ÄďMS. In another study, targeted LC‚ÄďMS/MS analyses on 832/13 cells demonstrated increases in ATP, GTP, NADH, NADPH, glutamine, glutamate, succinyl-CoA and malonyl-CoA pools after 45 min of glucose stimulation whereas adenosine, AMP, aspartate and HMG-CoA levels decreased. |
|
Formal Description Interaction-ID: 82069 |
process insulin secretion, second phase decreases_quantity of drug/chemical compound |
| Comment | The mitochondrial export of citrate and isocitrate and engagement of isocitrate with cytosolic, NADP-dependent isocitrate dehydrogenase (IDH1, ICDc) play a central role in regulation of GSIS. |
|
Formal Description Interaction-ID: 82070 |
affects_activity of |
| Comment | The mitochondrial export of citrate and isocitrate and engagement of isocitrate with cytosolic, NADP-dependent isocitrate dehydrogenase (IDH1, ICDc) play a central role in regulation of GSIS. |
|
Formal Description Interaction-ID: 82071 |
complex/PPI affects_activity of |
| Comment | NADPH generated by ICDc (IDH1) enhances exocytosis via signaling through reduced glutathione (GSH). Furthermore, intracellular provision of isocitrate, NADPH, or GSH rescues impaired exocytotic function in beta-cells from donors with T2D. Thus, the isocitrate-NADPH-GSH pathway represents an important link between glucose metabolism and insulin exocytosis. |
|
Formal Description Interaction-ID: 82072 |
complex/PPI increases_quantity of drug/chemical compound |
| Comment | NADPH generated by ICDc (IDH1) enhances exocytosis via signaling through reduced glutathione (GSH). Furthermore, intracellular provision of isocitrate, NADPH, or GSH rescues impaired exocytotic function in beta-cells from donors with T2D. Thus, the isocitrate-NADPH-GSH pathway represents an important link between glucose metabolism and insulin exocytosis. |
|
Formal Description Interaction-ID: 82073 |
drug/chemical compound increases_activity of process insulin granule exocytosis |
| Comment | NADPH generated by ICDc (IDH1) enhances exocytosis via signaling through reduced glutathione (GSH). Furthermore, intracellular provision of isocitrate, NADPH, or GSH rescues impaired exocytotic function in beta-cells from donors with T2D. Thus, the isocitrate-NADPH-GSH pathway represents an important link between glucose metabolism and insulin exocytosis. |
|
Formal Description Interaction-ID: 82074 |
drug/chemical compound increases_activity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for |
| Comment | NADPH generated by ICDc (IDH1) enhances exocytosis via signaling through reduced glutathione (GSH). Furthermore, intracellular provision of isocitrate, NADPH, or GSH rescues impaired exocytotic function in beta-cells from donors with T2D. Thus, the isocitrate-NADPH-GSH pathway represents an important link between glucose metabolism and insulin exocytosis. |
|
Formal Description Interaction-ID: 82075 |
drug/chemical compound increases_activity of process insulin granule exocytosis |
| Drugbank entries | Show/Hide entries for Glutathione |
| Comment | NADPH generated by ICDc (IDH1) enhances exocytosis via signaling through reduced glutathione (GSH). Furthermore, intracellular provision of isocitrate, NADPH, or GSH rescues impaired exocytotic function in beta-cells from donors with T2D. Thus, the isocitrate-NADPH-GSH pathway represents an important link between glucose metabolism and insulin exocytosis. |
|
Formal Description Interaction-ID: 82076 |
complex/PPI increases_activity of process insulin granule exocytosis |
| Comment | Free fatty acids play an important role in regulating beta-cell function under physiological conditions. Exposure to fatty acid is known to amplify GSIS, with maximal potentiation depending upon both fatty acid metabolism within the beta-cell and activation of the G-protein coupled receptor, FFAR1/GPR40. |
|
Formal Description Interaction-ID: 82077 |
|
| Comment | Free fatty acids play an important role in regulating beta-cell function under physiological conditions. Exposure to fatty acid is known to amplify GSIS, with maximal potentiation depending upon both fatty acid metabolism within the beta-cell and activation of the G-protein coupled receptor, FFAR1/GPR40. |
|
Formal Description Interaction-ID: 82078 |
drug/chemical compound increases_activity of |
| Comment | Free fatty acids play an important role in regulating beta-cell function under physiological conditions. Exposure to fatty acid is known to amplify GSIS, with maximal potentiation depending upon both fatty acid metabolism within the beta-cell and activation of the G-protein coupled receptor, FFAR1/GPR40. |
|
Formal Description Interaction-ID: 82079 |
gene/protein increases_activity of |
| Drugbank entries | Show/Hide entries for FFAR1 |
| Comment | Extensive LC‚ÄďMS/MS metabolite profiling and [U-13C]glucose flux analyses of 832/13 cells exposed to 0.5 mM palmitate showed a fatty acid-induced increase in long chain acyl-CoAs that were rapidly esterified with glucose-derived glycerol-3-phosphate to form lysophosphatidic acid, mono- and diacylglycerols, and other glycerolipids. Exposure to fatty acids also caused a surprising increase in glycolytic flux, along with a reduction in the NADH/NAD ratio. Using pulse-chase experiments, the authors demonstrated that increased glycolytic flux was due to enhanced conversion of dihydroxyacetone phosphate to glycerol-3-phosphate (NADH dependent) driven by the fatty acid-mediated increase in glycerol-3-phosphate consumption. |
|
Formal Description Interaction-ID: 82080 |
drug/chemical compound increases_quantity of drug/chemical compound |
| Comment | Extensive LC‚ÄďMS/MS metabolite profiling and [U-13C]glucose flux analyses of 832/13 cells exposed to 0.5 mM palmitate showed a fatty acid-induced increase in long chain acyl-CoAs that were rapidly esterified with glucose-derived glycerol-3-phosphate to form lysophosphatidic acid, mono- and diacylglycerols, and other glycerolipids. Exposure to fatty acids also caused a surprising increase in glycolytic flux, along with a reduction in the NADH/NAD ratio. Using pulse-chase experiments, the authors demonstrated that increased glycolytic flux was due to enhanced conversion of dihydroxyacetone phosphate to glycerol-3-phosphate (NADH dependent) driven by the fatty acid-mediated increase in glycerol-3-phosphate consumption. |
|
Formal Description Interaction-ID: 82081 |
drug/chemical compound increases_quantity of drug/chemical compound |
| Comment | Extensive LC‚ÄďMS/MS metabolite profiling and [U-13C]glucose flux analyses of 832/13 cells exposed to 0.5 mM palmitate showed a fatty acid-induced increase in long chain acyl-CoAs that were rapidly esterified with glucose-derived glycerol-3-phosphate to form lysophosphatidic acid, mono- and diacylglycerols, and other glycerolipids. Exposure to fatty acids also caused a surprising increase in glycolytic flux, along with a reduction in the NADH/NAD ratio. Using pulse-chase experiments, the authors demonstrated that increased glycolytic flux was due to enhanced conversion of dihydroxyacetone phosphate to glycerol-3-phosphate (NADH dependent) driven by the fatty acid-mediated increase in glycerol-3-phosphate consumption. |
|
Formal Description Interaction-ID: 82082 |
drug/chemical compound increases_quantity of drug/chemical compound |
| Comment | Extensive LC‚ÄďMS/MS metabolite profiling and [U-13C]glucose flux analyses of 832/13 cells exposed to 0.5 mM palmitate showed a fatty acid-induced increase in long chain acyl-CoAs that were rapidly esterified with glucose-derived glycerol-3-phosphate to form lysophosphatidic acid, mono- and diacylglycerols, and other glycerolipids. Exposure to fatty acids also caused a surprising increase in glycolytic flux, along with a reduction in the NADH/NAD ratio. Using pulse-chase experiments, the authors demonstrated that increased glycolytic flux was due to enhanced conversion of dihydroxyacetone phosphate to glycerol-3-phosphate (NADH dependent) driven by the fatty acid-mediated increase in glycerol-3-phosphate consumption. |
|
Formal Description Interaction-ID: 82083 |
drug/chemical compound increases_quantity of drug/chemical compound |
| Comment | Extensive LC‚ÄďMS/MS metabolite profiling and [U-13C]glucose flux analyses of 832/13 cells exposed to 0.5 mM palmitate showed a fatty acid-induced increase in long chain acyl-CoAs that were rapidly esterified with glucose-derived glycerol-3-phosphate to form lysophosphatidic acid, mono- and diacylglycerols, and other glycerolipids. Exposure to fatty acids also caused a surprising increase in glycolytic flux, along with a reduction in the NADH/NAD ratio. Using pulse-chase experiments, the authors demonstrated that increased glycolytic flux was due to enhanced conversion of dihydroxyacetone phosphate to glycerol-3-phosphate (NADH dependent) driven by the fatty acid-mediated increase in glycerol-3-phosphate consumption. |
|
Formal Description Interaction-ID: 82084 |
drug/chemical compound increases_activity of process |
| Comment | Vesicular glutamate transporter-1 is essential for incretin-mediated insulin secretion. Cytosolic glutamate derived from glucose through the malate-aspartate shuttle is a signaling factor in incretin-induced insulin secretion. |
|
Formal Description Interaction-ID: 82085 |
gene/protein increases_activity of process insulin secretion, incretin-induced |
| Comment | Vesicular glutamate transporter-1 is essential for incretin-mediated insulin secretion. Cytosolic glutamate derived from glucose through the malate-aspartate shuttle is a signaling factor in incretin-induced insulin secretion. |
|
Formal Description Interaction-ID: 82086 |
|
| Comment | Vesicular glutamate transporter-1 is essential for incretin-mediated insulin secretion. Cytosolic glutamate derived from glucose through the malate-aspartate shuttle is a signaling factor in incretin-induced insulin secretion. |
|
Formal Description Interaction-ID: 82087 |
process increases_quantity of drug/chemical compound |
| Comment | Vesicular glutamate transporter-1 is essential for incretin-mediated insulin secretion. Cytosolic glutamate derived from glucose through the malate-aspartate shuttle is a signaling factor in incretin-induced insulin secretion. |
|
Formal Description Interaction-ID: 82088 |
process decreases_quantity of drug/chemical compound |
| Comment | Vesicular glutamate transporter-1 is essential for incretin-mediated insulin secretion. Cytosolic glutamate derived from glucose through the malate-aspartate shuttle is a signaling factor in incretin-induced insulin secretion. |
|
Formal Description Interaction-ID: 82089 |
drug/chemical compound increases_activity of process insulin secretion, incretin-induced |
| Comment | Glycolysis and TCA cycle intermediates accumulate when cells are exposed to chronic hyperglycemia. |
|
Formal Description Interaction-ID: 82090 |
|
| Comment | Glycolysis and TCA cycle intermediates accumulate when cells are exposed to chronic hyperglycemia. |
|
Formal Description Interaction-ID: 82091 |
phenotype increases_activity of process |
| Comment | Similar to glucotoxicity, inhibition of 6PGDH inhibits insulin gene expression, GSIS and causes PPP intermediates to accumulate. Both glucotoxic conditions and 6PGDH inhibition have a similar effect to activate ERK1/2, and an ERK inhibitor attenuates glucose-induced PPP intermediate accumulation and GSIS inhibition, supporting the hypothesis that metabolites derived from the PPP activate ERK1/2 and contribute to the decline in beta-cell function. |
|
Formal Description Interaction-ID: 82092 |
phenotype increases_activity of process |
| Comment | Similar to glucotoxicity, inhibition of 6PGDH inhibits insulin gene expression, GSIS and causes PPP intermediates to accumulate. Both glucotoxic conditions and 6PGDH inhibition have a similar effect to activate ERK1/2, and an ERK inhibitor attenuates glucose-induced PPP intermediate accumulation and GSIS inhibition, supporting the hypothesis that metabolites derived from the PPP activate ERK1/2 and contribute to the decline in beta-cell function. |
|
Formal Description Interaction-ID: 82093 |
process increases_activity of process |
| Comment | Similar to glucotoxicity, inhibition of 6PGDH inhibits insulin gene expression, GSIS and causes PPP intermediates to accumulate. Both glucotoxic conditions and 6PGDH inhibition have a similar effect to activate ERK1/2, and an ERK inhibitor attenuates glucose-induced PPP intermediate accumulation and GSIS inhibition, supporting the hypothesis that metabolites derived from the PPP activate ERK1/2 and contribute to the decline in beta-cell function. |
|
Formal Description Interaction-ID: 82094 |
process decreases_activity of |
| Comment | Chronic exposure to hyperglycemia caused glutamine concentrations and C4-glutamate labeling from U-13C-glucose to decrease, while GABA concentrations increased. These changes may indicate changes in flux through the GABA shunt pathway and glutamate dehydrogenase which have both been implicated in beta-cell function. While this study did not investigate the mechanism of these changes, the results partly align with another report that employed the GABA transaminase inhibitor gabaculine and succinic semialdehyde supplementation of the GABA shunt to link GABA metabolism to GSIS in rat islets. |
|
Formal Description Interaction-ID: 82095 |
phenotype decreases_quantity of drug/chemical compound |
| Comment | Chronic exposure to hyperglycemia caused glutamine concentrations and C4-glutamate labeling from U-13C-glucose to decrease, while GABA concentrations increased. These changes may indicate changes in flux through the GABA shunt pathway and glutamate dehydrogenase which have both been implicated in beta-cell function. While this study did not investigate the mechanism of these changes, the results partly align with another report that employed the GABA transaminase inhibitor gabaculine and succinic semialdehyde supplementation of the GABA shunt to link GABA metabolism to GSIS in rat islets. |
|
Formal Description Interaction-ID: 82096 |
phenotype decreases_quantity of drug/chemical compound |
| Comment | Chronic exposure to hyperglycemia caused glutamine concentrations and C4-glutamate labeling from U-13C-glucose to decrease, while GABA concentrations increased. These changes may indicate changes in flux through the GABA shunt pathway and glutamate dehydrogenase which have both been implicated in beta-cell function. While this study did not investigate the mechanism of these changes, the results partly align with another report that employed the GABA transaminase inhibitor gabaculine and succinic semialdehyde supplementation of the GABA shunt to link GABA metabolism to GSIS in rat islets. |
|
Formal Description Interaction-ID: 82097 |
|
| Comment | Chronic exposure to hyperglycemia caused glutamine concentrations and C4-glutamate labeling from U-13C-glucose to decrease, while GABA concentrations increased. These changes may indicate changes in flux through the GABA shunt pathway and glutamate dehydrogenase which have both been implicated in beta-cell function. While this study did not investigate the mechanism of these changes, the results partly align with another report that employed the GABA transaminase inhibitor gabaculine and succinic semialdehyde supplementation of the GABA shunt to link GABA metabolism to GSIS in rat islets. |
|
Formal Description Interaction-ID: 82098 |
affects_activity of |
| Comment | Chronic exposure to hyperglycemia caused glutamine concentrations and C4-glutamate labeling from U-13C-glucose to decrease, while GABA concentrations increased. These changes may indicate changes in flux through the GABA shunt pathway and glutamate dehydrogenase which have both been implicated in beta-cell function. While this study did not investigate the mechanism of these changes, the results partly align with another report that employed the GABA transaminase inhibitor gabaculine and succinic semialdehyde supplementation of the GABA shunt to link GABA metabolism to GSIS in rat islets. |
|
Formal Description Interaction-ID: 82099 |
gene/protein affects_activity of |
| Drugbank entries | Show/Hide entries for GLUD1 |
| Comment | Glucotoxic conditions increase expression of lipogenic genes, activate fatty acid synthesis and elevate total fatty acid concentrations. A parallel decrease in phosphocholine concentrations has also been observed. One study reported a glucose-induced reduction in percent composition of low abundance polyunsaturated fatty acids (PUFAs), whereas another study found no change in percent composition for high-abundance fatty acids over a variety of chain lengths and saturation levels. |
|
Formal Description Interaction-ID: 82100 |
phenotype increases_activity of process |
| Comment | Glucotoxic conditions increase expression of lipogenic genes, activate fatty acid synthesis and elevate total fatty acid concentrations. A parallel decrease in phosphocholine concentrations has also been observed. One study reported a glucose-induced reduction in percent composition of low abundance polyunsaturated fatty acids (PUFAs), whereas another study found no change in percent composition for high-abundance fatty acids over a variety of chain lengths and saturation levels. |
|
Formal Description Interaction-ID: 82101 |
phenotype increases_quantity of drug/chemical compound |
| Comment | Glucotoxic conditions increase expression of lipogenic genes, activate fatty acid synthesis and elevate total fatty acid concentrations. A parallel decrease in phosphocholine concentrations has also been observed. One study reported a glucose-induced reduction in percent composition of low abundance polyunsaturated fatty acids (PUFAs), whereas another study found no change in percent composition for high-abundance fatty acids over a variety of chain lengths and saturation levels. |
|
Formal Description Interaction-ID: 82102 |
phenotype decreases_quantity of drug/chemical compound |
| Comment | Glucotoxic conditions increase expression of lipogenic genes, activate fatty acid synthesis and elevate total fatty acid concentrations. A parallel decrease in phosphocholine concentrations has also been observed. One study reported a glucose-induced reduction in percent composition of low abundance polyunsaturated fatty acids (PUFAs), whereas another study found no change in percent composition for high-abundance fatty acids over a variety of chain lengths and saturation levels. |
|
Formal Description Interaction-ID: 82103 |
phenotype decreases_quantity of drug/chemical compound Polyunsaturated fatty acid |
| Comment | Lipidomics analysis of INS-1E cells pre-exposed to intermediate periods of hyperglycemia (16 h at 16 mM glucose), demonstrated decreased PUFA content, including arachidonic acid and linoleic acid, higher monounsaturated fatty acid content and higher concentrations of 4-hydroxy-2E-nonenal (4-HNE) a product of arachidonic acid oxidation via a non-enzymatic route. Relative abundance of n-3 PUFAs increased while n-6 PUFAs decreased. These changes occurred in parallel with a compensatory increase in insulin secretion, increased phosphorylation and activation of calcium-dependent phospholipase A2 (cPLA2), and accumulation of reactive oxygen species. |
|
Formal Description Interaction-ID: 82104 |
phenotype decreases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for |
| Comment | Lipidomics analysis of INS-1E cells pre-exposed to intermediate periods of hyperglycemia (16 h at 16 mM glucose), demonstrated decreased PUFA content, including arachidonic acid and linoleic acid, higher monounsaturated fatty acid content and higher concentrations of 4-hydroxy-2E-nonenal (4-HNE) a product of arachidonic acid oxidation via a non-enzymatic route. Relative abundance of n-3 PUFAs increased while n-6 PUFAs decreased. These changes occurred in parallel with a compensatory increase in insulin secretion, increased phosphorylation and activation of calcium-dependent phospholipase A2 (cPLA2), and accumulation of reactive oxygen species. |
|
Formal Description Interaction-ID: 82105 |
phenotype decreases_quantity of drug/chemical compound |
| Comment | Lipidomics analysis of INS-1E cells pre-exposed to intermediate periods of hyperglycemia (16 h at 16 mM glucose), demonstrated decreased PUFA content, including arachidonic acid and linoleic acid, higher monounsaturated fatty acid content and higher concentrations of 4-hydroxy-2E-nonenal (4-HNE) a product of arachidonic acid oxidation via a non-enzymatic route. Relative abundance of n-3 PUFAs increased while n-6 PUFAs decreased. These changes occurred in parallel with a compensatory increase in insulin secretion, increased phosphorylation and activation of calcium-dependent phospholipase A2 (cPLA2), and accumulation of reactive oxygen species. |
|
Formal Description Interaction-ID: 82106 |
phenotype increases_quantity of drug/chemical compound Monounsaturated fatty acid |
| Comment | Lipidomics analysis of INS-1E cells pre-exposed to intermediate periods of hyperglycemia (16 h at 16 mM glucose), demonstrated decreased PUFA content, including arachidonic acid and linoleic acid, higher monounsaturated fatty acid content and higher concentrations of 4-hydroxy-2E-nonenal (4-HNE) a product of arachidonic acid oxidation via a non-enzymatic route. Relative abundance of n-3 PUFAs increased while n-6 PUFAs decreased. These changes occurred in parallel with a compensatory increase in insulin secretion, increased phosphorylation and activation of calcium-dependent phospholipase A2 (cPLA2), and accumulation of reactive oxygen species. |
|
Formal Description Interaction-ID: 82107 |
phenotype increases_quantity of drug/chemical compound |
| Comment | Lipidomics analysis of INS-1E cells pre-exposed to intermediate periods of hyperglycemia (16 h at 16 mM glucose), demonstrated decreased PUFA content, including arachidonic acid and linoleic acid, higher monounsaturated fatty acid content and higher concentrations of 4-hydroxy-2E-nonenal (4-HNE) a product of arachidonic acid oxidation via a non-enzymatic route. Relative abundance of n-3 PUFAs increased while n-6 PUFAs decreased. These changes occurred in parallel with a compensatory increase in insulin secretion, increased phosphorylation and activation of calcium-dependent phospholipase A2 (cPLA2), and accumulation of reactive oxygen species. |
|
Formal Description Interaction-ID: 82108 |
drug/chemical compound increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for Arachidonic acid |
| Comment | Lipidomics analysis of INS-1E cells pre-exposed to intermediate periods of hyperglycemia (16 h at 16 mM glucose), demonstrated decreased PUFA content, including arachidonic acid and linoleic acid, higher monounsaturated fatty acid content and higher concentrations of 4-hydroxy-2E-nonenal (4-HNE) a product of arachidonic acid oxidation via a non-enzymatic route. Relative abundance of n-3 PUFAs increased while n-6 PUFAs decreased. These changes occurred in parallel with a compensatory increase in insulin secretion, increased phosphorylation and activation of calcium-dependent phospholipase A2 (cPLA2), and accumulation of reactive oxygen species. |
|
Formal Description Interaction-ID: 82109 |
phenotype increases_activity of gene/protein |
| Drugbank entries | Show/Hide entries for PLA2G4A |
| Comment | Supplementation of 4-HNE activated PPARdelta and GSIS in a dose dependent manner, and these effects were inhibited by the antioxidant N-acetylcysteine and PPARdelta antagonist GSK0660. PPARdelta activity potentiated by 4-HNE may therefore have an amplifying effect on insulin secretion during beta-cell adaptation to intermediate hyperglycemic exposure. |
|
Formal Description Interaction-ID: 82110 |
drug/chemical compound increases_activity of gene/protein |
| Drugbank entries | Show/Hide entries for PPARD |
| Comment | Supplementation of 4-HNE activated PPARdelta and GSIS in a dose dependent manner, and these effects were inhibited by the antioxidant N-acetylcysteine and PPARdelta antagonist GSK0660. PPARdelta activity potentiated by 4-HNE may therefore have an amplifying effect on insulin secretion during beta-cell adaptation to intermediate hyperglycemic exposure. |
|
Formal Description Interaction-ID: 82111 |
drug/chemical compound increases_activity of |
| Comment | Prolonged exposure to fatty acids in the presence of intermediate glucose can impair beta-cell function. |
|
Formal Description Interaction-ID: 82112 |
|
| Comment | A lipidomic profile of Min6 cells treated with 0.4 mM palmitate in the presence of 6 mM glucose for 48 h found increases in total phosphatidylcholine, di-, and triacylglycerol content with enhanced incorporation of palmitate, but no significant changes in total cholesterol esters or cholesterol saturation index. Phosphatidylethanolamine pools were 50% higher in response to palmitate. In the sphingolipid class, pools of glucosylceramide, lactosylceramide, and trihexosylceramide increased with palmitate, while ceramide and sphingomyelin pools were unchanged. Unsaturated and long chain glucosylceramide variants also accumulated with palmitate treatment. A more detailed analysis of lipid species in the subcellular fractions of the same Min6 model identified a significant rise in the ceramide pools in the ER and lysosome fractions, an increase in the glycosylceramide pools of the ER and plasma membrane, and a decrease in sphingomyelin and free cholesterol content in the ER. An independent laboratory found sphingosine-1-phosphate and dihydrosphingosine-1-phosphate accumulated upon chronic palmitate exposure in INS-1 cells. |
|
Formal Description Interaction-ID: 82113 |
drug/chemical compound increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for Palmitic acid |
| Comment | A lipidomic profile of Min6 cells treated with 0.4 mM palmitate in the presence of 6 mM glucose for 48 h found increases in total phosphatidylcholine, di-, and triacylglycerol content with enhanced incorporation of palmitate, but no significant changes in total cholesterol esters or cholesterol saturation index. Phosphatidylethanolamine pools were 50% higher in response to palmitate. In the sphingolipid class, pools of glucosylceramide, lactosylceramide, and trihexosylceramide increased with palmitate, while ceramide and sphingomyelin pools were unchanged. Unsaturated and long chain glucosylceramide variants also accumulated with palmitate treatment. A more detailed analysis of lipid species in the subcellular fractions of the same Min6 model identified a significant rise in the ceramide pools in the ER and lysosome fractions, an increase in the glycosylceramide pools of the ER and plasma membrane, and a decrease in sphingomyelin and free cholesterol content in the ER. An independent laboratory found sphingosine-1-phosphate and dihydrosphingosine-1-phosphate accumulated upon chronic palmitate exposure in INS-1 cells. |
|
Formal Description Interaction-ID: 82114 |
drug/chemical compound increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for Palmitic acid |
| Comment | A lipidomic profile of Min6 cells treated with 0.4 mM palmitate in the presence of 6 mM glucose for 48 h found increases in total phosphatidylcholine, di-, and triacylglycerol content with enhanced incorporation of palmitate, but no significant changes in total cholesterol esters or cholesterol saturation index. Phosphatidylethanolamine pools were 50% higher in response to palmitate. In the sphingolipid class, pools of glucosylceramide, lactosylceramide, and trihexosylceramide increased with palmitate, while ceramide and sphingomyelin pools were unchanged. Unsaturated and long chain glucosylceramide variants also accumulated with palmitate treatment. A more detailed analysis of lipid species in the subcellular fractions of the same Min6 model identified a significant rise in the ceramide pools in the ER and lysosome fractions, an increase in the glycosylceramide pools of the ER and plasma membrane, and a decrease in sphingomyelin and free cholesterol content in the ER. An independent laboratory found sphingosine-1-phosphate and dihydrosphingosine-1-phosphate accumulated upon chronic palmitate exposure in INS-1 cells. |
|
Formal Description Interaction-ID: 82115 |
drug/chemical compound increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for Palmitic acid |
| Comment | A lipidomic profile of Min6 cells treated with 0.4 mM palmitate in the presence of 6 mM glucose for 48 h found increases in total phosphatidylcholine, di-, and triacylglycerol content with enhanced incorporation of palmitate, but no significant changes in total cholesterol esters or cholesterol saturation index. Phosphatidylethanolamine pools were 50% higher in response to palmitate. In the sphingolipid class, pools of glucosylceramide, lactosylceramide, and trihexosylceramide increased with palmitate, while ceramide and sphingomyelin pools were unchanged. Unsaturated and long chain glucosylceramide variants also accumulated with palmitate treatment. A more detailed analysis of lipid species in the subcellular fractions of the same Min6 model identified a significant rise in the ceramide pools in the ER and lysosome fractions, an increase in the glycosylceramide pools of the ER and plasma membrane, and a decrease in sphingomyelin and free cholesterol content in the ER. An independent laboratory found sphingosine-1-phosphate and dihydrosphingosine-1-phosphate accumulated upon chronic palmitate exposure in INS-1 cells. |
|
Formal Description Interaction-ID: 82116 |
drug/chemical compound increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for Palmitic acid or Phosphatidylethanolamine |
| Comment | A lipidomic profile of Min6 cells treated with 0.4 mM palmitate in the presence of 6 mM glucose for 48 h found increases in total phosphatidylcholine, di-, and triacylglycerol content with enhanced incorporation of palmitate, but no significant changes in total cholesterol esters or cholesterol saturation index. Phosphatidylethanolamine pools were 50% higher in response to palmitate. In the sphingolipid class, pools of glucosylceramide, lactosylceramide, and trihexosylceramide increased with palmitate, while ceramide and sphingomyelin pools were unchanged. Unsaturated and long chain glucosylceramide variants also accumulated with palmitate treatment. A more detailed analysis of lipid species in the subcellular fractions of the same Min6 model identified a significant rise in the ceramide pools in the ER and lysosome fractions, an increase in the glycosylceramide pools of the ER and plasma membrane, and a decrease in sphingomyelin and free cholesterol content in the ER. An independent laboratory found sphingosine-1-phosphate and dihydrosphingosine-1-phosphate accumulated upon chronic palmitate exposure in INS-1 cells. |
|
Formal Description Interaction-ID: 82117 |
drug/chemical compound increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for Palmitic acid |
| Comment | A lipidomic profile of Min6 cells treated with 0.4 mM palmitate in the presence of 6 mM glucose for 48 h found increases in total phosphatidylcholine, di-, and triacylglycerol content with enhanced incorporation of palmitate, but no significant changes in total cholesterol esters or cholesterol saturation index. Phosphatidylethanolamine pools were 50% higher in response to palmitate. In the sphingolipid class, pools of glucosylceramide, lactosylceramide, and trihexosylceramide increased with palmitate, while ceramide and sphingomyelin pools were unchanged. Unsaturated and long chain glucosylceramide variants also accumulated with palmitate treatment. A more detailed analysis of lipid species in the subcellular fractions of the same Min6 model identified a significant rise in the ceramide pools in the ER and lysosome fractions, an increase in the glycosylceramide pools of the ER and plasma membrane, and a decrease in sphingomyelin and free cholesterol content in the ER. An independent laboratory found sphingosine-1-phosphate and dihydrosphingosine-1-phosphate accumulated upon chronic palmitate exposure in INS-1 cells. |
|
Formal Description Interaction-ID: 82118 |
drug/chemical compound increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for Palmitic acid |
| Comment | A lipidomic profile of Min6 cells treated with 0.4 mM palmitate in the presence of 6 mM glucose for 48 h found increases in total phosphatidylcholine, di-, and triacylglycerol content with enhanced incorporation of palmitate, but no significant changes in total cholesterol esters or cholesterol saturation index. Phosphatidylethanolamine pools were 50% higher in response to palmitate. In the sphingolipid class, pools of glucosylceramide, lactosylceramide, and trihexosylceramide increased with palmitate, while ceramide and sphingomyelin pools were unchanged. Unsaturated and long chain glucosylceramide variants also accumulated with palmitate treatment. A more detailed analysis of lipid species in the subcellular fractions of the same Min6 model identified a significant rise in the ceramide pools in the ER and lysosome fractions, an increase in the glycosylceramide pools of the ER and plasma membrane, and a decrease in sphingomyelin and free cholesterol content in the ER. An independent laboratory found sphingosine-1-phosphate and dihydrosphingosine-1-phosphate accumulated upon chronic palmitate exposure in INS-1 cells. |
|
Formal Description Interaction-ID: 82119 |
drug/chemical compound increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for Palmitic acid |
| Comment | A lipidomic profile of Min6 cells treated with 0.4 mM palmitate in the presence of 6 mM glucose for 48 h found increases in total phosphatidylcholine, di-, and triacylglycerol content with enhanced incorporation of palmitate, but no significant changes in total cholesterol esters or cholesterol saturation index. Phosphatidylethanolamine pools were 50% higher in response to palmitate. In the sphingolipid class, pools of glucosylceramide, lactosylceramide, and trihexosylceramide increased with palmitate, while ceramide and sphingomyelin pools were unchanged. Unsaturated and long chain glucosylceramide variants also accumulated with palmitate treatment. A more detailed analysis of lipid species in the subcellular fractions of the same Min6 model identified a significant rise in the ceramide pools in the ER and lysosome fractions, an increase in the glycosylceramide pools of the ER and plasma membrane, and a decrease in sphingomyelin and free cholesterol content in the ER. An independent laboratory found sphingosine-1-phosphate and dihydrosphingosine-1-phosphate accumulated upon chronic palmitate exposure in INS-1 cells. |
|
Formal Description Interaction-ID: 82120 |
drug/chemical compound increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for Palmitic acid |
| Comment | A lipidomic profile of Min6 cells treated with 0.4 mM palmitate in the presence of 6 mM glucose for 48 h found increases in total phosphatidylcholine, di-, and triacylglycerol content with enhanced incorporation of palmitate, but no significant changes in total cholesterol esters or cholesterol saturation index. Phosphatidylethanolamine pools were 50% higher in response to palmitate. In the sphingolipid class, pools of glucosylceramide, lactosylceramide, and trihexosylceramide increased with palmitate, while ceramide and sphingomyelin pools were unchanged. Unsaturated and long chain glucosylceramide variants also accumulated with palmitate treatment. A more detailed analysis of lipid species in the subcellular fractions of the same Min6 model identified a significant rise in the ceramide pools in the ER and lysosome fractions, an increase in the glycosylceramide pools of the ER and plasma membrane, and a decrease in sphingomyelin and free cholesterol content in the ER. An independent laboratory found sphingosine-1-phosphate and dihydrosphingosine-1-phosphate accumulated upon chronic palmitate exposure in INS-1 cells. |
|
Formal Description Interaction-ID: 82121 |
drug/chemical compound increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for Palmitic acid |
| Comment | Sphingomyelin and cholesterol are co-regulated by palmitate and colocalize in lipid rafts. Palmitate promoted ER lipid raft formation in Min6 cells and islets, slowed ER-to-Golgi protein trafficking, and enhanced apoptosis. |
|
Formal Description Interaction-ID: 82122 |
|
| Drugbank entries | Show/Hide entries for Palmitic acid |
| Comment | Sphingomyelin and cholesterol are co-regulated by palmitate and colocalize in lipid rafts. Palmitate promoted ER lipid raft formation in Min6 cells and islets, slowed ER-to-Golgi protein trafficking, and enhanced apoptosis. |
|
Formal Description Interaction-ID: 82123 |
|
| Drugbank entries | Show/Hide entries for Palmitic acid or Cholesterol |
| Comment | Sphingomyelin and cholesterol are co-regulated by palmitate and colocalize in lipid rafts. Palmitate promoted ER lipid raft formation in Min6 cells and islets, slowed ER-to-Golgi protein trafficking, and enhanced apoptosis. |
|
Formal Description Interaction-ID: 82124 |
|
| Comment | Sphingomyelin and cholesterol are co-regulated by palmitate and colocalize in lipid rafts. Palmitate promoted ER lipid raft formation in Min6 cells and islets, slowed ER-to-Golgi protein trafficking, and enhanced apoptosis. |
|
Formal Description Interaction-ID: 82125 |
|
| Drugbank entries | Show/Hide entries for Cholesterol |
| Comment | Sphingomyelin and cholesterol are co-regulated by palmitate and colocalize in lipid rafts. Palmitate promoted ER lipid raft formation in Min6 cells and islets, slowed ER-to-Golgi protein trafficking, and enhanced apoptosis. |
|
Formal Description Interaction-ID: 82126 |
drug/chemical compound increases_quantity of cellular component ER membrane raft |
| Drugbank entries | Show/Hide entries for Palmitic acid |
| Comment | Sphingomyelin and cholesterol are co-regulated by palmitate and colocalize in lipid rafts. Palmitate promoted ER lipid raft formation in Min6 cells and islets, slowed ER-to-Golgi protein trafficking, and enhanced apoptosis. |
|
Formal Description Interaction-ID: 82127 |
drug/chemical compound increases_activity of process ER membrane raft organization |
| Drugbank entries | Show/Hide entries for Palmitic acid |
| Comment | Sphingomyelin and cholesterol are co-regulated by palmitate and colocalize in lipid rafts. Palmitate promoted ER lipid raft formation in Min6 cells and islets, slowed ER-to-Golgi protein trafficking, and enhanced apoptosis. |
|
Formal Description Interaction-ID: 82128 |
drug/chemical compound decreases_activity of |
| Drugbank entries | Show/Hide entries for Palmitic acid |
| Comment | Sphingomyelin and cholesterol are co-regulated by palmitate and colocalize in lipid rafts. Palmitate promoted ER lipid raft formation in Min6 cells and islets, slowed ER-to-Golgi protein trafficking, and enhanced apoptosis. |
|
Formal Description Interaction-ID: 82129 |
drug/chemical compound increases_activity of process |
| Drugbank entries | Show/Hide entries for Palmitic acid |
| Comment | Inhibition of serine palmitoyltransferase 1, the enzyme that catalyzes the first step of ceramide synthesis, inhibits induction of CHOP and activation of caspase 3 in response to palmitate, implicating ceramide synthesis in lipotoxic ER stress and apoptosis. |
|
Formal Description Interaction-ID: 82130 |
complex/PPI Serine palmitoyltransferase 1 increases_activity of process |
| Comment | Inhibition of serine palmitoyltransferase 1, the enzyme that catalyzes the first step of ceramide synthesis, inhibits induction of CHOP and activation of caspase 3 in response to palmitate, implicating ceramide synthesis in lipotoxic ER stress and apoptosis. |
|
Formal Description Interaction-ID: 82131 |
|
| Comment | Inhibition of serine palmitoyltransferase 1, the enzyme that catalyzes the first step of ceramide synthesis, inhibits induction of CHOP and activation of caspase 3 in response to palmitate, implicating ceramide synthesis in lipotoxic ER stress and apoptosis. |
|
Formal Description Interaction-ID: 82132 |
|
| Drugbank entries | Show/Hide entries for CASP3 |
| Comment | Expression of sphingosine kinase 1 (SphK1), an ER localized enzyme, is induced by palmitate, and SphK1 overexpression potentiates dihydrosphingosine-1-phosphate accumulation while attenuating accumulation of multiple ceramides. Pharmacological inhibition of SphK1 increases caspase 3/7 activation in response to palmitate exposure. SphK1 overexpression also partly protects against the palmitate induced ER-to-Golgi trafficking defect and apoptosis. |
|
Formal Description Interaction-ID: 82133 |
|
| Drugbank entries | Show/Hide entries for Palmitic acid |
| Comment | Expression of sphingosine kinase 1 (SphK1), an ER localized enzyme, is induced by palmitate, and SphK1 overexpression potentiates dihydrosphingosine-1-phosphate accumulation while attenuating accumulation of multiple ceramides. Pharmacological inhibition of SphK1 increases caspase 3/7 activation in response to palmitate exposure. SphK1 overexpression also partly protects against the palmitate induced ER-to-Golgi trafficking defect and apoptosis. |
|
Formal Description Interaction-ID: 82134 |
|
| Comment | Expression of sphingosine kinase 1 (SphK1), an ER localized enzyme, is induced by palmitate, and SphK1 overexpression potentiates dihydrosphingosine-1-phosphate accumulation while attenuating accumulation of multiple ceramides. Pharmacological inhibition of SphK1 increases caspase 3/7 activation in response to palmitate exposure. SphK1 overexpression also partly protects against the palmitate induced ER-to-Golgi trafficking defect and apoptosis. |
|
Formal Description Interaction-ID: 82135 |
gene/protein affects_activity of |
| Comment | Expression of sphingosine kinase 1 (SphK1), an ER localized enzyme, is induced by palmitate, and SphK1 overexpression potentiates dihydrosphingosine-1-phosphate accumulation while attenuating accumulation of multiple ceramides. Pharmacological inhibition of SphK1 increases caspase 3/7 activation in response to palmitate exposure. SphK1 overexpression also partly protects against the palmitate induced ER-to-Golgi trafficking defect and apoptosis. |
|
Formal Description Interaction-ID: 82136 |
|
| Comment | Sphingomyelin synthase 1 (SMS1) overexpression attenuated palmitate-induced apoptosis, while sphingomyelinase Smpd4 potentiated it. |
|
Formal Description Interaction-ID: 82137 |
|
| Comment | Sphingomyelin synthase 1 (SMS1) overexpression attenuated palmitate-induced apoptosis, while sphingomyelinase Smpd4 potentiated it. |
|
Formal Description Interaction-ID: 82138 |
|
| Drugbank entries | Show/Hide entries for SMPD4 |