CIDeRplusGeneral Information:
| Id: | 1,092 |
| Diseases: |
Diabetes mellitus, type II
- [OMIM]
Insulin resistance Obesity - [OMIM] |
| Mammalia | |
| article | |
| Reference: | de Luca C and Olefsky JM(2008) Inflammation and insulin resistance FEBS Lett. 582: 97-105 [PMID: 18053812] |
Interaction Information:
| Comment | In skeletal muscle insulin promotes glucose uptake by stimulating translocation of the GLUT4 glucose transporter to the plasma membrane, and impaired skeletal muscle insulin signaling results in decreased glucose disposal. |
|
Formal Description Interaction-ID: 6917 |
|
| Comment | In skeletal muscle insulin promotes glucose uptake by stimulating translocation of the GLUT4 glucose transporter to the plasma membrane, and impaired skeletal muscle insulin signaling results in decreased glucose disposal. |
|
Formal Description Interaction-ID: 6923 |
|
| Comment | In skeletal muscle insulin promotes glucose uptake by stimulating translocation of the GLUT4 glucose transporter to the plasma membrane, and impaired skeletal muscle insulin signaling results in decreased glucose disposal. |
|
Formal Description Interaction-ID: 6925 |
|
| Comment | In the liver, insulin inhibits the expression of key gluconeogenic enzymes and, therefore, insulin resistance in liver leads to elevated hepatic glucose production. |
|
Formal Description Interaction-ID: 6926 |
|
| Comment | In the liver, insulin inhibits the expression of key gluconeogenic enzymes and, therefore, insulin resistance in liver leads to elevated hepatic glucose production. |
|
Formal Description Interaction-ID: 6928 |
|
| Comment | Adipose tissue insulin signaling results in decreased hormone sensitive lipase activity and this anti-lipolytic effect inhibits free fatty acid (FFA) efflux out of adipocytes. |
|
Formal Description Interaction-ID: 6929 |
|
| Comment | Adipose tissue insulin signaling results in decreased hormone sensitive lipase activity and this anti-lipolytic effect inhibits free fatty acid (FFA) efflux out of adipocytes. |
|
Formal Description Interaction-ID: 6931 |
|
| Comment | Adipose tissue insulin signaling results in decreased hormone sensitive lipase activity and this anti-lipolytic effect inhibits free fatty acid (FFA) efflux out of adipocytes. |
|
Formal Description Interaction-ID: 6932 |
|
| Comment | Increased circulating FFA can result in decreased insulin sensitivity in skeletal muscle due to an increase in intracellular lipid products, including fatty acyl-CoA and ceramide. These lipid intermediates can activate the serine/threonine kinase, protein kinase C-theta (PKC-theta), which then inhibits the insulin signaling cascade. |
|
Formal Description Interaction-ID: 6933 |
affects_quantity of drug/chemical compound |
| Comment | Increased circulating FFA can result in decreased insulin sensitivity in skeletal muscle due to an increase in intracellular lipid products, including fatty acyl-CoA and ceramide. These lipid intermediates can activate the serine/threonine kinase, protein kinase C-theta (PKC-theta), which then inhibits the insulin signaling cascade. |
|
Formal Description Interaction-ID: 6960 |
|
| Drugbank entries | Show/Hide entries for PRKCQ |
| Comment | Increased circulating FFA can result in decreased insulin sensitivity in skeletal muscle due to an increase in intracellular lipid products, including fatty acyl-CoA and ceramide. These lipid intermediates can activate the serine/threonine kinase, protein kinase C-theta (PKC-theta), which then inhibits the insulin signaling cascade. |
|
Formal Description Interaction-ID: 6962 |
gene/protein decreases_activity of |
| Drugbank entries | Show/Hide entries for PRKCQ |
| Comment | Increased circulating FFA can result in decreased insulin sensitivity in skeletal muscle due to an increase in intracellular lipid products, including fatty acyl-CoA and ceramide. These lipid intermediates can activate the serine/threonine kinase, protein kinase C-theta (PKC-theta), which then inhibits the insulin signaling cascade. |
|
Formal Description Interaction-ID: 6963 |
|
| Drugbank entries | Show/Hide entries for PRKCQ |
| Comment | The insulin signaling cascade branches off into two main pathways, the first is the phosphatidylinositol 3-kinase (PI3K)-AKT (also called protein kinase B (PKB)) pathway which is largely responsible for insulin action on glucose uptake, as well as other metabolic actions of insulin, including the suppression of gluconeogenesis. The second pathway is the Ras-mitogen activated protein kinase (MAPK) pathway which mediates gene expression, but also interacts with the PI3K-AKT pathway to control cell growth and differentiation. |
|
Formal Description Interaction-ID: 6964 |
increases_activity of |
| Comment | The insulin signaling cascade branches off into two main pathways, the first is the phosphatidylinositol 3-kinase (PI3K)-AKT (also called protein kinase B (PKB)) pathway which is largely responsible for insulin action on glucose uptake, as well as other metabolic actions of insulin, including the suppression of gluconeogenesis. The second pathway is the Ras-mitogen activated protein kinase (MAPK) pathway which mediates gene expression, but also interacts with the PI3K-AKT pathway to control cell growth and differentiation. |
|
Formal Description Interaction-ID: 6966 |
affects_activity of process |
| Comment | The insulin signaling cascade branches off into two main pathways, the first is the phosphatidylinositol 3-kinase (PI3K)-AKT (also called protein kinase B (PKB)) pathway which is largely responsible for insulin action on glucose uptake, as well as other metabolic actions of insulin, including the suppression of gluconeogenesis. The second pathway is the Ras-mitogen activated protein kinase (MAPK) pathway which mediates gene expression, but also interacts with the PI3K-AKT pathway to control cell growth and differentiation. |
|
Formal Description Interaction-ID: 6967 |
decreases_activity of process |
| Comment | The insulin signaling cascade branches off into two main pathways, the first is the phosphatidylinositol 3-kinase (PI3K)-AKT (also called protein kinase B (PKB)) pathway which is largely responsible for insulin action on glucose uptake, as well as other metabolic actions of insulin, including the suppression of gluconeogenesis. The second pathway is the Ras-mitogen activated protein kinase (MAPK) pathway which mediates gene expression, but also interacts with the PI3K-AKT pathway to control cell growth and differentiation. |
|
Formal Description Interaction-ID: 6968 |
increases_activity of process |
| Comment | The insulin signaling cascade branches off into two main pathways, the first is the phosphatidylinositol 3-kinase (PI3K)-AKT (also called protein kinase B (PKB)) pathway which is largely responsible for insulin action on glucose uptake, as well as other metabolic actions of insulin, including the suppression of gluconeogenesis. The second pathway is the Ras-mitogen activated protein kinase (MAPK) pathway which mediates gene expression, but also interacts with the PI3K-AKT pathway to control cell growth and differentiation. |
|
Formal Description Interaction-ID: 6971 |
|
| Comment | The insulin signaling cascade branches off into two main pathways, the first is the phosphatidylinositol 3-kinase (PI3K)-AKT (also called protein kinase B (PKB)) pathway which is largely responsible for insulin action on glucose uptake, as well as other metabolic actions of insulin, including the suppression of gluconeogenesis. The second pathway is the Ras-mitogen activated protein kinase (MAPK) pathway which mediates gene expression, but also interacts with the PI3K-AKT pathway to control cell growth and differentiation. |
|
Formal Description Interaction-ID: 6973 |
process affects_activity of |
| Comment | The insulin signaling cascade branches off into two main pathways, the first is the phosphatidylinositol 3-kinase (PI3K)-AKT (also called protein kinase B (PKB)) pathway which is largely responsible for insulin action on glucose uptake, as well as other metabolic actions of insulin, including the suppression of gluconeogenesis. The second pathway is the Ras-mitogen activated protein kinase (MAPK) pathway which mediates gene expression, but also interacts with the PI3K-AKT pathway to control cell growth and differentiation. |
|
Formal Description Interaction-ID: 6974 |
|
| Comment | The insulin signaling cascade branches off into two main pathways, the first is the phosphatidylinositol 3-kinase (PI3K)-AKT (also called protein kinase B (PKB)) pathway which is largely responsible for insulin action on glucose uptake, as well as other metabolic actions of insulin, including the suppression of gluconeogenesis. The second pathway is the Ras-mitogen activated protein kinase (MAPK) pathway which mediates gene expression, but also interacts with the PI3K-AKT pathway to control cell growth and differentiation. |
|
Formal Description Interaction-ID: 6975 |
|
| Comment | Activation of the insulin receptor leads to tyrosine phosphorylation of IRS1 thereby initiating signal transduction. |
|
Formal Description Interaction-ID: 6980 |
|
| Drugbank entries | Show/Hide entries for IRS1 |
| Comment | Activation of the insulin receptor leads to tyrosine phosphorylation of IRS1 thereby initiating signal transduction. |
|
Formal Description Interaction-ID: 6981 |
|
| Comment | When IRS1 is alternatively phosphorylated on serine 307, its downstream signaling ability is diminished. Serine kinases that phosphorylate serine 307 include I kappa B kinase beta (Ikkb) in the NFkappaB pathway and C-jun N-terminal kinase 1 (Jnk1) in the JNK/AP-1 pathway. |
|
Formal Description Interaction-ID: 6982 |
|
| Drugbank entries | Show/Hide entries for IKBKB or IRS1 |
| Comment | When IRS1 is alternatively phosphorylated on serine 307, its downstream signaling ability is diminished. Serine kinases that phosphorylate serine 307 include I kappa B kinase beta (Ikkb) in the NFkappaB pathway and C-jun N-terminal kinase 1 (Jnk1) in the JNK/AP-1 pathway. |
|
Formal Description Interaction-ID: 6983 |
|
| Drugbank entries | Show/Hide entries for MAPK8 or IRS1 |
| Comment | When IRS1 is alternatively phosphorylated on serine 307, its downstream signaling ability is diminished. Serine kinases that phosphorylate serine 307 include I kappa B kinase beta (Ikkb) in the NFkappaB pathway and C-jun N-terminal kinase 1 (Jnk1) in the JNK/AP-1 pathway. |
|
Formal Description Interaction-ID: 6984 |
protein modification IRS1-phosSer307 decreases_activity of |
| Comment | Socs1 and Socs3, which are induced in inflammation, promote the ubiquitylation and subsequent degradation of IRS1. |
|
Formal Description Interaction-ID: 6985 |
|
| Comment | Socs1 and Socs3, which are induced in inflammation, promote the ubiquitylation and subsequent degradation of IRS1. |
|
Formal Description Interaction-ID: 6999 |
|
| Comment | Socs1 and Socs3, which are induced in inflammation, promote the ubiquitylation and subsequent degradation of IRS1. |
|
Formal Description Interaction-ID: 7001 |
|
| Drugbank entries | Show/Hide entries for IRS1 |
| Comment | Socs1 and Socs3, which are induced in inflammation, promote the ubiquitylation and subsequent degradation of IRS1. |
|
Formal Description Interaction-ID: 7003 |
|
| Drugbank entries | Show/Hide entries for IRS1 |
| Comment | Socs1 and Socs3, which are induced in inflammation, promote the ubiquitylation and subsequent degradation of IRS1. |
|
Formal Description Interaction-ID: 7004 |
|
| Drugbank entries | Show/Hide entries for IRS1 |
| Comment | Socs1 and Socs3, which are induced in inflammation, promote the ubiquitylation and subsequent degradation of IRS1. |
|
Formal Description Interaction-ID: 7005 |
|
| Drugbank entries | Show/Hide entries for IRS1 |
| Comment | The activated insulin receptor can phosphorylate tyrosine residues on Src homology 2 containing protein (Shc) which then binds to the Son of sevenless (SOS)-growth factor receptor-bound protein 2 (Grb2) complex which then triggers the Ras-MAPK signaling cascade. |
|
Formal Description Interaction-ID: 7008 |
complex/PPI Insulin receptor increases_phosphorylation of gene/protein SHC |
| Drugbank entries | Show/Hide entries for SHC |
| Comment | The activated insulin receptor can phosphorylate tyrosine residues on Src homology 2 containing protein (Shc) which then binds to the Son of sevenless (SOS)-growth factor receptor-bound protein 2 (Grb2) complex which then triggers the Ras-MAPK signaling cascade. |
|
Formal Description Interaction-ID: 7009 |
|
| Drugbank entries | Show/Hide entries for GRB2 |
| Comment | The activated insulin receptor can phosphorylate tyrosine residues on Src homology 2 containing protein (Shc) which then binds to the Son of sevenless (SOS)-growth factor receptor-bound protein 2 (Grb2) complex which then triggers the Ras-MAPK signaling cascade. |
|
Formal Description Interaction-ID: 7011 |
|
| Comment | An additional mediator of insulin action is the heterotrimeric G protein, G-alpha-q/11. Phosphorylation of G-alpha-q/11 by the insulin receptor activates PI3K, thus, stimulating GLUT4-mediated glucose uptake. This signaling pathway is inhibited by G-protein-coupled receptor kinase-2 (Grk2) which binds and inhibits the G-alpha subunit of G-alpha-q/11. |
|
Formal Description Interaction-ID: 7013 |
complex/PPI Insulin receptor increases_phosphorylation of complex/PPI G-alpha-q/11 complex |
| Comment | An additional mediator of insulin action is the heterotrimeric G protein, G-alpha-q/11. Phosphorylation of G-alpha-q/11 by the insulin receptor activates PI3K, thus, stimulating GLUT4-mediated glucose uptake. This signaling pathway is inhibited by G-protein-coupled receptor kinase-2 (Grk2) which binds and inhibits the G-alpha subunit of G-alpha-q/11. |
|
Formal Description Interaction-ID: 7041 |
complex/PPI Insulin receptor increases_activity of complex/PPI G-alpha-q/11 complex |
| Comment | An additional mediator of insulin action is the heterotrimeric G protein, G-alpha-q/11. Phosphorylation of G-alpha-q/11 by the insulin receptor activates PI3K, thus, stimulating GLUT4-mediated glucose uptake. This signaling pathway is inhibited by G-protein-coupled receptor kinase-2 (Grk2) which binds and inhibits the G-alpha subunit of G-alpha-q/11. |
|
Formal Description Interaction-ID: 7042 |
complex/PPI G-alpha-q/11 complex increases_activity of complex/PPI Phosphatidylinositol 3-kinase |
| Comment | An additional mediator of insulin action is the heterotrimeric G protein, G-alpha-q/11. Phosphorylation of G-alpha-q/11 by the insulin receptor activates PI3K, thus, stimulating GLUT4-mediated glucose uptake. This signaling pathway is inhibited by G-protein-coupled receptor kinase-2 (Grk2) which binds and inhibits the G-alpha subunit of G-alpha-q/11. |
|
Formal Description Interaction-ID: 7043 |
|
| Comment | An additional mediator of insulin action is the heterotrimeric G protein, G-alpha-q/11. Phosphorylation of G-alpha-q/11 by the insulin receptor activates PI3K, thus, stimulating GLUT4-mediated glucose uptake. This signaling pathway is inhibited by G-protein-coupled receptor kinase-2 (Grk2) which binds and inhibits the G-alpha subunit of G-alpha-q/11. |
|
Formal Description Interaction-ID: 7044 |
|
| Comment | The proto-oncogene product, Cbl, is recruited to the insulin receptor by the adapter protein Cbl associated protein (CAP) and the CAP/Cbl complex can mediate cell surface translocation of GLUT4 independent of PI3K activity. |
|
Formal Description Interaction-ID: 7060 |
complex/PPI Insulin receptor increases_activity of complex/PPI CAP-CBL complex |
| Comment | The proto-oncogene product, Cbl, is recruited to the insulin receptor by the adapter protein Cbl associated protein (CAP) and the CAP/Cbl complex can mediate cell surface translocation of GLUT4 independent of PI3K activity. |
|
Formal Description Interaction-ID: 7061 |
complex/PPI CAP-CBL complex increases_activity of gene/protein |
| Comment | The proto-oncogene product, Cbl, is recruited to the insulin receptor by the adapter protein Cbl associated protein (CAP) and the CAP/Cbl complex can mediate cell surface translocation of GLUT4 independent of PI3K activity. |
|
Formal Description Interaction-ID: 7062 |
complex/PPI CAP-CBL complex increases_activity of process |
| Comment | Elevated levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin (IL-8) have all been reported in various diabetic and insulin resistant states. |
|
Formal Description Interaction-ID: 7063 |
cooccurs with disease Insulin resistance |
| Comment | Elevated levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin (IL-8) have all been reported in various diabetic and insulin resistant states. |
|
Formal Description Interaction-ID: 7064 |
|
| Comment | Elevated levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin (IL-8) have all been reported in various diabetic and insulin resistant states. |
|
Formal Description Interaction-ID: 7065 |
phenotype increased circulating interleukin-8 level cooccurs with disease Insulin resistance |
| Comment | The inflammatory marker C-reactive protein (CRP), a non-specific acute phase reactant, is commonly elevated in human insulin resistant states. |
|
Formal Description Interaction-ID: 7066 |
phenotype increased circulating C-reactive protein level cooccurs with disease Insulin resistance |
| Comment | The inflammatory marker C-reactive protein (CRP), a non-specific acute phase reactant, is commonly elevated in human insulin resistant states. |
|
Formal Description Interaction-ID: 7067 |
process increases_activity of phenotype increased circulating C-reactive protein level |
| Comment | Adipokines such as resistin, leptin and adiponectin, which are secreted by adipocytes, can also affect inflammation and insulin sensitivity. |
|
Formal Description Interaction-ID: 7068 |
|
| Comment | Adipokines such as resistin, leptin and adiponectin, which are secreted by adipocytes, can also affect inflammation and insulin sensitivity. |
|
Formal Description Interaction-ID: 7069 |
|
| Comment | Adipokines such as resistin, leptin and adiponectin, which are secreted by adipocytes, can also affect inflammation and insulin sensitivity. |
|
Formal Description Interaction-ID: 7070 |
|
| Comment | Adipokines such as resistin, leptin and adiponectin, which are secreted by adipocytes, can also affect inflammation and insulin sensitivity. |
|
Formal Description Interaction-ID: 7071 |
|
| Comment | Adipokines such as resistin, leptin and adiponectin, which are secreted by adipocytes, can also affect inflammation and insulin sensitivity. |
|
Formal Description Interaction-ID: 7072 |
|
| Comment | Adipokines such as resistin, leptin and adiponectin, which are secreted by adipocytes, can also affect inflammation and insulin sensitivity. |
|
Formal Description Interaction-ID: 7073 |
|
| Comment | Hepatic inflammation can occur in obesity whereby inflammatory pathway activation could be the result of steatosis and/or increased hepatocyte stress pathway responses. This can result in hepatocyte-autonomous inflammation. Kupffer cells (liver-resident macrophage-like cells) can also become activated, releasing locally acting cytokines which further exacerbates inflammation and hepatic insulin resistance. |
|
Formal Description Interaction-ID: 7075 |
|
| Comment | Hepatic inflammation can occur in obesity whereby inflammatory pathway activation could be the result of steatosis and/or increased hepatocyte stress pathway responses. This can result in hepatocyte-autonomous inflammation. Kupffer cells (liver-resident macrophage-like cells) can also become activated, releasing locally acting cytokines which further exacerbates inflammation and hepatic insulin resistance. |
|
Formal Description Interaction-ID: 7076 |
|
| Comment | Hepatic inflammation can occur in obesity whereby inflammatory pathway activation could be the result of steatosis and/or increased hepatocyte stress pathway responses. This can result in hepatocyte-autonomous inflammation. Kupffer cells (liver-resident macrophage-like cells) can also become activated, releasing locally acting cytokines which further exacerbates inflammation and hepatic insulin resistance. |
|
Formal Description Interaction-ID: 7077 |
|
| Comment | Hepatic inflammation can occur in obesity whereby inflammatory pathway activation could be the result of steatosis and/or increased hepatocyte stress pathway responses. This can result in hepatocyte-autonomous inflammation. Kupffer cells (liver-resident macrophage-like cells) can also become activated, releasing locally acting cytokines which further exacerbates inflammation and hepatic insulin resistance. |
|
Formal Description Interaction-ID: 7078 |
tissue/cell line increases_activity of |
| Comment | Hepatic inflammation can occur in obesity whereby inflammatory pathway activation could be the result of steatosis and/or increased hepatocyte stress pathway responses. This can result in hepatocyte-autonomous inflammation. Kupffer cells (liver-resident macrophage-like cells) can also become activated, releasing locally acting cytokines which further exacerbates inflammation and hepatic insulin resistance. |
|
Formal Description Interaction-ID: 7081 |
increases_activity of disease Insulin resistance |
| Comment | Overnutrition and obesity are often accompanied by elevations in tissue and circulating FFA concentrations, and saturated FFAs can directly activate pro-inflammatory responses in vascular endothelial cells, adipocytes and myeloid-derived cells. The result of these obesity-induced physiologic events is the development of systemic inflammation. |
|
Formal Description Interaction-ID: 7082 |
|
| Comment | Overnutrition and obesity are often accompanied by elevations in tissue and circulating FFA concentrations, and saturated FFAs can directly activate pro-inflammatory responses in vascular endothelial cells, adipocytes and myeloid-derived cells. The result of these obesity-induced physiologic events is the development of systemic inflammation. |
|
Formal Description Interaction-ID: 7083 |
increases_activity of process |
| Comment | Tnf (a.k.a. Tnf-alpha) is a pro-inflammatory cytokine secreted predominantly by monocytes and macrophages. Activation of the Tnf receptor results in stimulation of NF-kappa-B signaling via Ikkb. |
|
Formal Description Interaction-ID: 7084 |
|
| Drugbank entries | Show/Hide entries for TNF or TNFRSF1A |
| Comment | Tnf (a.k.a. Tnf-alpha) is a pro-inflammatory cytokine secreted predominantly by monocytes and macrophages. Activation of the Tnf receptor results in stimulation of NF-kappa-B signaling via Ikkb. |
|
Formal Description Interaction-ID: 7085 |
|
| Drugbank entries | Show/Hide entries for TNFRSF1A or IKBKB |
| Comment | Tnf (a.k.a. Tnf-alpha) is a pro-inflammatory cytokine secreted predominantly by monocytes and macrophages. Activation of the Tnf receptor results in stimulation of NF-kappa-B signaling via Ikkb. |
|
Formal Description Interaction-ID: 7086 |
|
| Drugbank entries | Show/Hide entries for IKBKB |
| Comment | By activating Ikkb, Tnf stimulation leads to serine phosphorylation of Irs1 which attenuates its ability to transduce insulin mediated cellular events. |
|
Formal Description Interaction-ID: 7087 |
|
| Drugbank entries | Show/Hide entries for IKBKB or IRS1 |
| Comment | By activating Ikkb, Tnf stimulation leads to serine phosphorylation of Irs1 which attenuates its ability to transduce insulin mediated cellular events. |
|
Formal Description Interaction-ID: 7088 |
|
| Drugbank entries | Show/Hide entries for IKBKB or IRS1 |
| Comment | Treatment of cultured 3T3-L1 adipocytes with Tnf leads to reduced expression of the insulin receptor, IRS1 and Glut4 genes, as well as a decrease in insulin stimulated glucose uptake. |
|
Formal Description Interaction-ID: 7089 |
|
| Drugbank entries | Show/Hide entries for TNF or INSR |
| Comment | Treatment of cultured 3T3-L1 adipocytes with Tnf leads to reduced expression of the insulin receptor, IRS1 and Glut4 genes, as well as a decrease in insulin stimulated glucose uptake. |
|
Formal Description Interaction-ID: 7090 |
|
| Drugbank entries | Show/Hide entries for TNF or IRS1 |
| Comment | Treatment of cultured 3T3-L1 adipocytes with Tnf leads to reduced expression of the insulin receptor, IRS1 and Glut4 genes, as well as a decrease in insulin stimulated glucose uptake. |
|
Formal Description Interaction-ID: 7091 |
|
| Drugbank entries | Show/Hide entries for TNF |
| Comment | Treatment of cultured 3T3-L1 adipocytes with Tnf leads to reduced expression of the insulin receptor, IRS1 and Glut4 genes, as well as a decrease in insulin stimulated glucose uptake. |
|
Formal Description Interaction-ID: 7092 |
|
| Drugbank entries | Show/Hide entries for TNF |
| Comment | A Tnf-induced decrease in 3T3-L1 adipocyte genes has been found, including GLUT4, Hormone Sensitive Lipase (HSL), long-chain fatty acyl CoA synthetase, adiponectin (ADIPOQ), the transcription factor CCAAT/enhancer binding protein-alpha (C/EBP), and the nuclear receptors Pparg and retinoic acid x receptor (RXR). These genes all contribute to glucose homeostasis, both directly and indirectly. |
|
Formal Description Interaction-ID: 7093 |
|
| Drugbank entries | Show/Hide entries for TNF |
| Comment | A Tnf-induced decrease in 3T3-L1 adipocyte genes has been found, including GLUT4, Hormone Sensitive Lipase (HSL), long-chain fatty acyl CoA synthetase, adiponectin (ADIPOQ), the transcription factor CCAAT/enhancer binding protein-alpha (C/EBP), and the nuclear receptors Pparg and retinoic acid x receptor (RXR). These genes all contribute to glucose homeostasis, both directly and indirectly. |
|
Formal Description Interaction-ID: 7095 |
|
| Drugbank entries | Show/Hide entries for TNF |
| Comment | A Tnf-induced decrease in 3T3-L1 adipocyte genes has been found, including GLUT4, Hormone Sensitive Lipase (HSL), long-chain fatty acyl CoA synthetase, adiponectin (ADIPOQ), the transcription factor CCAAT/enhancer binding protein-alpha (C/EBP), and the nuclear receptors Pparg and retinoic acid x receptor (RXR). These genes all contribute to glucose homeostasis, both directly and indirectly. |
|
Formal Description Interaction-ID: 7096 |
|
| Drugbank entries | Show/Hide entries for TNF |
| Comment | A Tnf-induced decrease in 3T3-L1 adipocyte genes has been found, including GLUT4, Hormone Sensitive Lipase (HSL), long-chain fatty acyl CoA synthetase, adiponectin (ADIPOQ), the transcription factor CCAAT/enhancer binding protein-alpha (C/EBP), and the nuclear receptors Pparg and retinoic acid x receptor (RXR). These genes all contribute to glucose homeostasis, both directly and indirectly. |
|
Formal Description Interaction-ID: 7097 |
|
| Drugbank entries | Show/Hide entries for TNF |
| Comment | A Tnf-induced decrease in 3T3-L1 adipocyte genes has been found, including GLUT4, Hormone Sensitive Lipase (HSL), long-chain fatty acyl CoA synthetase, adiponectin (ADIPOQ), the transcription factor CCAAT/enhancer binding protein-alpha (C/EBP), and the nuclear receptors Pparg and retinoic acid x receptor (RXR). These genes all contribute to glucose homeostasis, both directly and indirectly. |
|
Formal Description Interaction-ID: 7098 |
|
| Drugbank entries | Show/Hide entries for TNF or PPARG |
| Comment | A Tnf-induced decrease in 3T3-L1 adipocyte genes has been found, including GLUT4, Hormone Sensitive Lipase (HSL), long-chain fatty acyl CoA synthetase, adiponectin (ADIPOQ), the transcription factor CCAAT/enhancer binding protein-alpha (C/EBP), and the nuclear receptors Pparg and retinoic acid x receptor (RXR). These genes all contribute to glucose homeostasis, both directly and indirectly. |
|
Formal Description Interaction-ID: 7099 |
|
| Drugbank entries | Show/Hide entries for TNF |
| Comment | A Tnf-induced decrease in 3T3-L1 adipocyte genes has been found, including GLUT4, Hormone Sensitive Lipase (HSL), long-chain fatty acyl CoA synthetase, adiponectin (ADIPOQ), the transcription factor CCAAT/enhancer binding protein-alpha (C/EBP), and the nuclear receptors Pparg and retinoic acid x receptor (RXR). These genes all contribute to glucose homeostasis, both directly and indirectly. |
|
Formal Description Interaction-ID: 7100 |
|
| Comment | A Tnf-induced decrease in 3T3-L1 adipocyte genes has been found, including GLUT4, Hormone Sensitive Lipase (HSL), long-chain fatty acyl CoA synthetase, adiponectin (ADIPOQ), the transcription factor CCAAT/enhancer binding protein-alpha (C/EBP), and the nuclear receptors Pparg and retinoic acid x receptor (RXR). These genes all contribute to glucose homeostasis, both directly and indirectly. |
|
Formal Description Interaction-ID: 7101 |
|
| Comment | A Tnf-induced decrease in 3T3-L1 adipocyte genes has been found, including GLUT4, Hormone Sensitive Lipase (HSL), long-chain fatty acyl CoA synthetase, adiponectin (ADIPOQ), the transcription factor CCAAT/enhancer binding protein-alpha (C/EBP), and the nuclear receptors Pparg and retinoic acid x receptor (RXR). These genes all contribute to glucose homeostasis, both directly and indirectly. |
|
Formal Description Interaction-ID: 7102 |
|
| Comment | A Tnf-induced decrease in 3T3-L1 adipocyte genes has been found, including GLUT4, Hormone Sensitive Lipase (HSL), long-chain fatty acyl CoA synthetase, adiponectin (ADIPOQ), the transcription factor CCAAT/enhancer binding protein-alpha (C/EBP), and the nuclear receptors Pparg and retinoic acid x receptor (RXR). These genes all contribute to glucose homeostasis, both directly and indirectly. |
|
Formal Description Interaction-ID: 7103 |
|
| Comment | A Tnf-induced decrease in 3T3-L1 adipocyte genes has been found, including GLUT4, Hormone Sensitive Lipase (HSL), long-chain fatty acyl CoA synthetase, adiponectin (ADIPOQ), the transcription factor CCAAT/enhancer binding protein-alpha (C/EBP), and the nuclear receptors Pparg and retinoic acid x receptor (RXR). These genes all contribute to glucose homeostasis, both directly and indirectly. |
|
Formal Description Interaction-ID: 7104 |
|
| Comment | A Tnf-induced decrease in 3T3-L1 adipocyte genes has been found, including GLUT4, Hormone Sensitive Lipase (HSL), long-chain fatty acyl CoA synthetase, adiponectin (ADIPOQ), the transcription factor CCAAT/enhancer binding protein-alpha (C/EBP), and the nuclear receptors Pparg and retinoic acid x receptor (RXR). These genes all contribute to glucose homeostasis, both directly and indirectly. |
|
Formal Description Interaction-ID: 7105 |
|
| Drugbank entries | Show/Hide entries for PPARG |
| Comment | A Tnf-induced decrease in 3T3-L1 adipocyte genes has been found, including GLUT4, Hormone Sensitive Lipase (HSL), long-chain fatty acyl CoA synthetase, adiponectin (ADIPOQ), the transcription factor CCAAT/enhancer binding protein-alpha (C/EBP), and the nuclear receptors Pparg and retinoic acid x receptor (RXR). These genes all contribute to glucose homeostasis, both directly and indirectly. |
|
Formal Description Interaction-ID: 7106 |
|
| Comment | Jnk1 (encoded by Mapk8) contributes to the development of insulin resistance in obese and diabetic states. |
|
Formal Description Interaction-ID: 7188 |
|
| Drugbank entries | Show/Hide entries for MAPK8 |
| Comment | Jnk1 knockout led to decreased IRS1 phospho-Ser307 in liver. |
|
Formal Description Interaction-ID: 7189 |
|
| Drugbank entries | Show/Hide entries for MAPK8 or IRS1 |
| Comment | The anti-inflammatory compounds, salicylate and its derivative aspirin,inhibit the activity of Ikkb, thus preventing Irs1 serine307 phosphorylation and this presumably accounts for their insulin-sensitizing effects. |
|
Formal Description Interaction-ID: 7190 |
|
| Drugbank entries | Show/Hide entries for IKBKB |
| Comment | The anti-inflammatory compounds, salicylate and its derivative aspirin,inhibit the activity of Ikkb, thus preventing Irs1 serine307 phosphorylation and this presumably accounts for their insulin-sensitizing effects. |
|
Formal Description Interaction-ID: 7193 |
|
| Drugbank entries | Show/Hide entries for IKBKB |
| Comment | The anti-inflammatory compounds, salicylate and its derivative aspirin,inhibit the activity of Ikkb, thus preventing Irs1 serine307 phosphorylation and this presumably accounts for their insulin-sensitizing effects. |
|
Formal Description Interaction-ID: 7195 |
|
| Comment | The anti-inflammatory compounds, salicylate and its derivative aspirin,inhibit the activity of Ikkb, thus preventing Irs1 serine307 phosphorylation and this presumably accounts for their insulin-sensitizing effects. |
|
Formal Description Interaction-ID: 7196 |
|
| Comment | Nitric oxide (NO) is an endogenous signaling molecule produced by nitric oxide synthase. NO acts as a signal transduction molecule for a number of physiological processes and is involved in many pathophysiologic states, including insulin resistance. |
|
Formal Description Interaction-ID: 7226 |
|
| Comment | Several inducers of insulin resistance, including FFAs, pro-inflammatory cytokines and oxidative stress, activate the expression of Nos2, the gene that encodes inducible nitric oxide synthase (iNOS). |
|
Formal Description Interaction-ID: 7229 |
increases_activity of disease Insulin resistance |
| Comment | Several inducers of insulin resistance, including FFAs, pro-inflammatory cytokines and oxidative stress, activate the expression of Nos2, the gene that encodes inducible nitric oxide synthase (iNOS). |
|
Formal Description Interaction-ID: 7230 |
gene/protein Proinflammatory cytokine increases_activity of disease Insulin resistance |
| Comment | Several inducers of insulin resistance, including FFAs, pro-inflammatory cytokines and oxidative stress, activate the expression of Nos2, the gene that encodes inducible nitric oxide synthase (iNOS). |
|
Formal Description Interaction-ID: 7238 |
|
| Comment | Several inducers of insulin resistance, including FFAs, pro-inflammatory cytokines and oxidative stress, activate the expression of Nos2, the gene that encodes inducible nitric oxide synthase (iNOS). |
|
Formal Description Interaction-ID: 7239 |
|
| Drugbank entries | Show/Hide entries for NOS2 |
| Comment | Several inducers of insulin resistance, including FFAs, pro-inflammatory cytokines and oxidative stress, activate the expression of Nos2, the gene that encodes inducible nitric oxide synthase (iNOS). |
|
Formal Description Interaction-ID: 7240 |
|
| Drugbank entries | Show/Hide entries for NOS2 |
| Comment | Several inducers of insulin resistance, including FFAs, pro-inflammatory cytokines and oxidative stress, activate the expression of Nos2, the gene that encodes inducible nitric oxide synthase (iNOS). |
|
Formal Description Interaction-ID: 7241 |
|
| Drugbank entries | Show/Hide entries for NOS2 |
| Comment | In the insulin signaling pathway, NO can reduce Akt activity by causing s-nitrosylation of a specific cysteine residue. |
|
Formal Description Interaction-ID: 7242 |
|
| Drugbank entries | Show/Hide entries for AKT1 |
| Comment | Increased iNOS activity also results in the degradation of Irs1 in cultured skeletal muscle cells. |
|
Formal Description Interaction-ID: 7244 |
|
| Drugbank entries | Show/Hide entries for NOS2 or IRS1 |
| Comment | Il-10 is an anti-inflammatory cytokine produced by macrophages and lymphocytes. Il-10 exerts its anti-inflammatory activity by inhibiting Tnf-induced NF-kappa-B activation by reducing IKK activity. |
|
Formal Description Interaction-ID: 7245 |
|
| Comment | Il-10 is an anti-inflammatory cytokine produced by macrophages and lymphocytes. Il-10 exerts its anti-inflammatory activity by inhibiting Tnf-induced NF-kappa-B activation by reducing IKK activity. |
|
Formal Description Interaction-ID: 7272 |
|
| Drugbank entries | Show/Hide entries for TNF |
| Comment | Il-10 is an anti-inflammatory cytokine produced by macrophages and lymphocytes. Il-10 exerts its anti-inflammatory activity by inhibiting Tnf-induced NF-kappa-B activation by reducing IKK activity. |
|
Formal Description Interaction-ID: 7273 |
|
| Comment | Il-10 is an anti-inflammatory cytokine produced by macrophages and lymphocytes. Il-10 exerts its anti-inflammatory activity by inhibiting Tnf-induced NF-kappa-B activation by reducing IKK activity. |
|
Formal Description Interaction-ID: 7274 |
|
| Comment | Il-10 is an anti-inflammatory cytokine produced by macrophages and lymphocytes. Il-10 exerts its anti-inflammatory activity by inhibiting Tnf-induced NF-kappa-B activation by reducing IKK activity. |
|
Formal Description Interaction-ID: 7276 |
|
| Comment | In human studies, it has been shown that there is a greater incidence of insulin resistance in subjects with reduced serum levels of IL-10. |
|
Formal Description Interaction-ID: 7277 |
increases_activity of disease Insulin resistance |
| Comment | A major conceptual advance in the field of obesity-induced inflammation and insulin resistance was made by the discovery of bone marrow-derived macrophages in adipose tissue of obese mice and humans. |
|
Formal Description Interaction-ID: 7278 |
|
| Comment | Adipose tissue macrophages are responsible for nearly all adipose tissue Tnf expression and a significant portion of Nos2 and Il6 expression. |
|
Formal Description Interaction-ID: 7281 |
|
| Drugbank entries | Show/Hide entries for TNF |
| Comment | Inactivation of myeloid-Ikkb activity prevents systemic insulin resistance, most likely by interrupting local paracrine effects between resident macrophages and insulin target tissues. |
|
Formal Description Interaction-ID: 7288 |
|
| Drugbank entries | Show/Hide entries for IKBKB |
| Comment | Newly recruited adipose tissue macrophages are pro-inflammatory, as indicated by increased expression of Il6, Nos2 and Ccr2, while resident adipose tissue macrophages are antiinflammatory. |
|
Formal Description Interaction-ID: 7291 |
tissue/cell line recruited adipose tissue macrophage increases_activity of process |
| Comment | Macrophages are also capable of undergoing a phenotypic switch from an M1 state, which was defined as the 'classically activated' pro-inflammatory macrophage, to the M2 state or the 'alternatively activated' non-inflammatory cell. The M2 classification involves cells that express arginase and the anti-inflammatory cytokine Il-10 and have a high capacity to repair damaged tissue. M1 cells express inflammatory cytokines and the cell surface marker Cd11c. Adipose tissue from obese mice contains proportionately more M1 macrophages, whereas, lean adipose tissue contains more M2 macrophages, and increased M1 content positively correlates with inflammation, macrophage infiltration and insulin resistance. |
|
Formal Description Interaction-ID: 7302 |
|
| Comment | Cbl-associated protein (CAP), known as a positive regulator of glucose transport into cells, plays a role in obesity-related inflammation due to its function in maintaining normal macrophage activity. |
|
Formal Description Interaction-ID: 7303 |
|
| Comment | Cbl-associated protein (CAP), known as a positive regulator of glucose transport into cells, plays a role in obesity-related inflammation due to its function in maintaining normal macrophage activity. |
|
Formal Description Interaction-ID: 7304 |
gene/protein increases_activity of process |
| Comment | Sorbs1 -/- mice show reduced activity of both Ikkb and Jnk, decreased Mcp1 protein levels, reduced macrophage infiltration and lower white blood cell counts. |
|
Formal Description Interaction-ID: 7307 |
|
| Drugbank entries | Show/Hide entries for IKBKB |
| Comment | Sorbs1 -/- mice show reduced activity of both Ikkb and Jnk, decreased Mcp1 protein levels, reduced macrophage infiltration and lower white blood cell counts. |
|
Formal Description Interaction-ID: 7309 |
|
| Drugbank entries | Show/Hide entries for MAPK8 |
| Comment | Sorbs1 -/- mice show reduced activity of both Ikkb and Jnk, decreased Mcp1 protein levels, reduced macrophage infiltration and lower white blood cell counts. |
|
Formal Description Interaction-ID: 7311 |
|
| Drugbank entries | Show/Hide entries for CCL2 |
| Comment | Pparg is a nuclear receptor required for adipogenesis. It is also the target for the insulin-sensitizing TZD class of drugs, which promote adipogenesis and cause systemic insulin sensitivity. |
|
Formal Description Interaction-ID: 7312 |
|
| Drugbank entries | Show/Hide entries for PPARG |
| Comment | Pparg is a nuclear receptor required for adipogenesis. It is also the target for the insulin-sensitizing TZD class of drugs, which promote adipogenesis and cause systemic insulin sensitivity. |
|
Formal Description Interaction-ID: 7314 |
|
| Comment | Pparg is a nuclear receptor required for adipogenesis. It is also the target for the insulin-sensitizing TZD class of drugs, which promote adipogenesis and cause systemic insulin sensitivity. |
|
Formal Description Interaction-ID: 7315 |
drug/chemical compound Thiazolidinedione decreases_activity of disease Insulin resistance |
| Comment | Pparg is a nuclear receptor required for adipogenesis. It is also the target for the insulin-sensitizing TZD class of drugs, which promote adipogenesis and cause systemic insulin sensitivity. |
|
Formal Description Interaction-ID: 7316 |
|
| Drugbank entries | Show/Hide entries for PPARG |
| Comment | In addition to adipocytes, Pparg is also expressed in macrophages where it negatively regulates a large set of inflammatory pathway genes by a unique transrepression mechanism. |
|
Formal Description Interaction-ID: 7317 |
|
| Drugbank entries | Show/Hide entries for PPARG |
| Comment | Jnk1 signaling in macrophages is a key component of macrophage function and a mediator of the macrophage inflammatory response which ultimately leads to insulin resistance. |
|
Formal Description Interaction-ID: 7319 |
|
| Drugbank entries | Show/Hide entries for MAPK8 |
| Comment | Jnk1 also plays an important role in non-hematopoietic cells in the development of obesity and the associated insulin resistance. |
|
Formal Description Interaction-ID: 7321 |
|
| Drugbank entries | Show/Hide entries for MAPK8 |
| Comment | Tlr4 belongs to the family of Toll-like receptors that function as pattern recognition receptors that guard against microorganismal infections as part of the innate immune system. Tlr4 is stimulated by lipopolysaccharide (LPS), an endotoxin released by gram-negative bacteria. Tlr4 stimulation results in the activation of both Ikkb/NF-kappa-B and JNK/AP-1 signaling, culminating in the expression and secretion of pro-inflammatory cytokines/chemokines, including, Il1b, IL-6, Tnf, Mcp1. |
|
Formal Description Interaction-ID: 7322 |
|
| Drugbank entries | Show/Hide entries for TLR4 |
| Comment | Tlr4 belongs to the family of Toll-like receptors that function as pattern recognition receptors that guard against microorganismal infections as part of the innate immune system. Tlr4 is stimulated by lipopolysaccharide (LPS), an endotoxin released by gram-negative bacteria. Tlr4 stimulation results in the activation of both Ikkb/NF-kappa-B and JNK/AP-1 signaling, culminating in the expression and secretion of pro-inflammatory cytokines/chemokines, including, Il1b, IL-6, Tnf, Mcp1. |
|
Formal Description Interaction-ID: 7323 |
|
| Drugbank entries | Show/Hide entries for TLR4 |
| Comment | Tlr4 belongs to the family of Toll-like receptors that function as pattern recognition receptors that guard against microorganismal infections as part of the innate immune system. Tlr4 is stimulated by lipopolysaccharide (LPS), an endotoxin released by gram-negative bacteria. Tlr4 stimulation results in the activation of both Ikkb/NF-kappa-B and JNK/AP-1 signaling, culminating in the expression and secretion of pro-inflammatory cytokines/chemokines, including, Il1b, IL-6, Tnf, Mcp1. |
|
Formal Description Interaction-ID: 7324 |
|
| Drugbank entries | Show/Hide entries for TLR4 |
| Comment | Tlr4 belongs to the family of Toll-like receptors that function as pattern recognition receptors that guard against microorganismal infections as part of the innate immune system. Tlr4 is stimulated by lipopolysaccharide (LPS), an endotoxin released by gram-negative bacteria. Tlr4 stimulation results in the activation of both Ikkb/NF-kappa-B and JNK/AP-1 signaling, culminating in the expression and secretion of pro-inflammatory cytokines/chemokines, including, Il1b, IL-6, Tnf, Mcp1. |
|
Formal Description Interaction-ID: 7325 |
|
| Drugbank entries | Show/Hide entries for TLR4 or IL1B |
| Comment | Tlr4 belongs to the family of Toll-like receptors that function as pattern recognition receptors that guard against microorganismal infections as part of the innate immune system. Tlr4 is stimulated by lipopolysaccharide (LPS), an endotoxin released by gram-negative bacteria. Tlr4 stimulation results in the activation of both Ikkb/NF-kappa-B and JNK/AP-1 signaling, culminating in the expression and secretion of pro-inflammatory cytokines/chemokines, including, Il1b, IL-6, Tnf, Mcp1. |
|
Formal Description Interaction-ID: 7326 |
|
| Drugbank entries | Show/Hide entries for TLR4 or IL6 |
| Comment | Tlr4 belongs to the family of Toll-like receptors that function as pattern recognition receptors that guard against microorganismal infections as part of the innate immune system. Tlr4 is stimulated by lipopolysaccharide (LPS), an endotoxin released by gram-negative bacteria. Tlr4 stimulation results in the activation of both Ikkb/NF-kappa-B and JNK/AP-1 signaling, culminating in the expression and secretion of pro-inflammatory cytokines/chemokines, including, Il1b, IL-6, Tnf, Mcp1. |
|
Formal Description Interaction-ID: 7327 |
|
| Drugbank entries | Show/Hide entries for TLR4 or TNF |
| Comment | Tlr4 belongs to the family of Toll-like receptors that function as pattern recognition receptors that guard against microorganismal infections as part of the innate immune system. Tlr4 is stimulated by lipopolysaccharide (LPS), an endotoxin released by gram-negative bacteria. Tlr4 stimulation results in the activation of both Ikkb/NF-kappa-B and JNK/AP-1 signaling, culminating in the expression and secretion of pro-inflammatory cytokines/chemokines, including, Il1b, IL-6, Tnf, Mcp1. |
|
Formal Description Interaction-ID: 7329 |
|
| Drugbank entries | Show/Hide entries for TLR4 or CCL2 |
| Comment | FFA activate the NF-kappa-B signaling pathway in primary macrophages from wildtype mice but not in macrophages derived from Tlr4 deficient (Tlr4-/-) mice. |
|
Formal Description Interaction-ID: 7347 |
drug/chemical compound increases_activity of |
| Comment | FFA activate the NF-kappa-B signaling pathway in primary macrophages from wildtype mice but not in macrophages derived from Tlr4 deficient (Tlr4-/-) mice. |
|
Formal Description Interaction-ID: 7352 |
drug/chemical compound NOT increases_activity of |
| Comment | Obese mice have increased Tlr4 expression in adipose tissue compared to lean controls. |
|
Formal Description Interaction-ID: 7353 |
|
| Drugbank entries | Show/Hide entries for TLR4 |
| Comment | The induction of ER stress induces insulin resistance via JNK-mediated serine phosphorylation of IRS1 in cultured liver cells. |
|
Formal Description Interaction-ID: 7354 |
increases_activity of disease Insulin resistance |
| Comment | The induction of ER stress induces insulin resistance via JNK-mediated serine phosphorylation of IRS1 in cultured liver cells. |
|
Formal Description Interaction-ID: 7356 |
|
| Drugbank entries | Show/Hide entries for MAPK8 |
| Comment | Newly recruited adipose tissue macrophages are pro-inflammatory, as indicated by increased expression of Il6, Nos2 and Ccr2, while resident adipose tissue macrophages are antiinflammatory. |
|
Formal Description Interaction-ID: 13444 |
tissue/cell line resident adipose tissue macrophage decreases_activity of process |
| Comment | In skeletal muscle insulin promotes glucose uptake by stimulating translocation of the GLUT4 glucose transporter to the plasma membrane, and impaired skeletal muscle insulin signaling results in decreased glucose disposal. |
|
Formal Description Interaction-ID: 16691 |
disease Insulin resistance decreases_activity of complex/PPI Insulin |
| Comment | Adipose tissue macrophages are responsible for nearly all adipose tissue Tnf expression and a significant portion of Nos2 and Il6 expression. |
|
Formal Description Interaction-ID: 45977 |
tissue/cell line adipose tissue macrophage increases_quantity of gene/protein |
| Drugbank entries | Show/Hide entries for NOS2 |
| Comment | Adipose tissue macrophages are responsible for nearly all adipose tissue Tnf expression and a significant portion of Nos2 and Il6 expression. |
|
Formal Description Interaction-ID: 45978 |
|
| Drugbank entries | Show/Hide entries for IL6 |
| Comment | Macrophages are also capable of undergoing a phenotypic switch from an M1 state, which was defined as the 'classically activated' pro-inflammatory macrophage, to the M2 state or the 'alternatively activated' non-inflammatory cell. The M2 classification involves cells that express arginase and the anti-inflammatory cytokine Il-10 and have a high capacity to repair damaged tissue. M1 cells express inflammatory cytokines and the cell surface marker Cd11c. Adipose tissue from obese mice contains proportionately more M1 macrophages, whereas, lean adipose tissue contains more M2 macrophages, and increased M1 content positively correlates with inflammation, macrophage infiltration and insulin resistance. |
|
Formal Description Interaction-ID: 45979 |
|
| Comment | Macrophages are also capable of undergoing a phenotypic switch from an M1 state, which was defined as the 'classically activated' pro-inflammatory macrophage, to the M2 state or the 'alternatively activated' non-inflammatory cell. The M2 classification involves cells that express arginase and the anti-inflammatory cytokine Il-10 and have a high capacity to repair damaged tissue. M1 cells express inflammatory cytokines and the cell surface marker Cd11c. Adipose tissue from obese mice contains proportionately more M1 macrophages, whereas, lean adipose tissue contains more M2 macrophages, and increased M1 content positively correlates with inflammation, macrophage infiltration and insulin resistance. |
|
Formal Description Interaction-ID: 45980 |
|
| Comment | Macrophages are also capable of undergoing a phenotypic switch from an M1 state, which was defined as the 'classically activated' pro-inflammatory macrophage, to the M2 state or the 'alternatively activated' non-inflammatory cell. The M2 classification involves cells that express arginase and the anti-inflammatory cytokine Il-10 and have a high capacity to repair damaged tissue. M1 cells express inflammatory cytokines and the cell surface marker Cd11c. Adipose tissue from obese mice contains proportionately more M1 macrophages, whereas, lean adipose tissue contains more M2 macrophages, and increased M1 content positively correlates with inflammation, macrophage infiltration and insulin resistance. |
|
Formal Description Interaction-ID: 45981 |
|
| Comment | Macrophages are also capable of undergoing a phenotypic switch from an M1 state, which was defined as the 'classically activated' pro-inflammatory macrophage, to the M2 state or the 'alternatively activated' non-inflammatory cell. The M2 classification involves cells that express arginase and the anti-inflammatory cytokine Il-10 and have a high capacity to repair damaged tissue. M1 cells express inflammatory cytokines and the cell surface marker Cd11c. Adipose tissue from obese mice contains proportionately more M1 macrophages, whereas, lean adipose tissue contains more M2 macrophages, and increased M1 content positively correlates with inflammation, macrophage infiltration and insulin resistance. |
|
Formal Description Interaction-ID: 45982 |
|
| Comment | Macrophages are also capable of undergoing a phenotypic switch from an M1 state, which was defined as the 'classically activated' pro-inflammatory macrophage, to the M2 state or the 'alternatively activated' non-inflammatory cell. The M2 classification involves cells that express arginase and the anti-inflammatory cytokine Il-10 and have a high capacity to repair damaged tissue. M1 cells express inflammatory cytokines and the cell surface marker Cd11c. Adipose tissue from obese mice contains proportionately more M1 macrophages, whereas, lean adipose tissue contains more M2 macrophages, and increased M1 content positively correlates with inflammation, macrophage infiltration and insulin resistance. |
|
Formal Description Interaction-ID: 45983 |
|
| Comment | Macrophages are also capable of undergoing a phenotypic switch from an M1 state, which was defined as the 'classically activated' pro-inflammatory macrophage, to the M2 state or the 'alternatively activated' non-inflammatory cell. The M2 classification involves cells that express arginase and the anti-inflammatory cytokine Il-10 and have a high capacity to repair damaged tissue. M1 cells express inflammatory cytokines and the cell surface marker Cd11c. Adipose tissue from obese mice contains proportionately more M1 macrophages, whereas, lean adipose tissue contains more M2 macrophages, and increased M1 content positively correlates with inflammation, macrophage infiltration and insulin resistance. |
|
Formal Description Interaction-ID: 45984 |
|
| Comment | Macrophages are also capable of undergoing a phenotypic switch from an M1 state, which was defined as the 'classically activated' pro-inflammatory macrophage, to the M2 state or the 'alternatively activated' non-inflammatory cell. The M2 classification involves cells that express arginase and the anti-inflammatory cytokine Il-10 and have a high capacity to repair damaged tissue. M1 cells express inflammatory cytokines and the cell surface marker Cd11c. Adipose tissue from obese mice contains proportionately more M1 macrophages, whereas, lean adipose tissue contains more M2 macrophages, and increased M1 content positively correlates with inflammation, macrophage infiltration and insulin resistance. |
|
Formal Description Interaction-ID: 45985 |
|