CIDeRplusGeneral Information:
| Id: | 8,614 |
| Diseases: |
Diabetes mellitus, type II
- [OMIM]
Insulin resistance |
| Mus musculus | |
| article | |
| Reference: | Fujisaka S et al.(2018) Diet, Genetics, and the Gut Microbiome Drive Dynamic Changes in Plasma Metabolites Cell Rep 22: 3072-3086 [PMID: 29539432] |
Interaction Information:
| Comment | To assess the effects of diet and antibiotics on the gut microbiota and metabolism, 6-week-old normal chow-fed (22% fat by calories) B6J, 129J, and 129T mice were given drinking water (placebo) or drinking water containing vancomycin (1 g/L) or metronidazole (1 g/L). One week later, both antibiotic-treated groups and half of the control mice were challenged with an HFD (60% fat by calories) for 4 weeks. Principal-component analysis of 16S rRNA sequence data of cecal contents showed clear differences in community structure between the different experimental groups, with both HFD and antibiotic treatment having a strong effect on the bacterial structure, with lesser but clear differences among strains. At the phylum level, the relative abundance of Firmicutes to Bacteroidetes was higher in both chow-fed 129 strains compared to B6J mice. HFD feeding reduced Bacteroidetes in all strains of mice. Both antibiotics resulted in elimination of most of the bacteria, except for Firmicutes in B6J and 129J mice, whereas, in 129T mice, considerable Proteobacteria and Verrucomicrobia remained. |
|
Formal Description Interaction-ID: 88844 |
environment antibiotic intake decreases_activity of environment gut flora diversity |
| Comment | To assess the effects of diet and antibiotics on the gut microbiota and metabolism, 6-week-old normal chow-fed (22% fat by calories) B6J, 129J, and 129T mice were given drinking water (placebo) or drinking water containing vancomycin (1 g/L) or metronidazole (1 g/L). One week later, both antibiotic-treated groups and half of the control mice were challenged with an HFD (60% fat by calories) for 4 weeks. Principal-component analysis of 16S rRNA sequence data of cecal contents showed clear differences in community structure between the different experimental groups, with both HFD and antibiotic treatment having a strong effect on the bacterial structure, with lesser but clear differences among strains. At the phylum level, the relative abundance of Firmicutes to Bacteroidetes was higher in both chow-fed 129 strains compared to B6J mice. HFD feeding reduced Bacteroidetes in all strains of mice. Both antibiotics resulted in elimination of most of the bacteria, except for Firmicutes in B6J and 129J mice, whereas, in 129T mice, considerable Proteobacteria and Verrucomicrobia remained. |
|
Formal Description Interaction-ID: 89071 |
environment high-fat diet affects_activity of environment gut flora diversity |
| Comment | To assess the effects of diet and antibiotics on the gut microbiota and metabolism, 6-week-old normal chow-fed (22% fat by calories) B6J, 129J, and 129T mice were given drinking water (placebo) or drinking water containing vancomycin (1 g/L) or metronidazole (1 g/L). One week later, both antibiotic-treated groups and half of the control mice were challenged with an HFD (60% fat by calories) for 4 weeks. Principal-component analysis of 16S rRNA sequence data of cecal contents showed clear differences in community structure between the different experimental groups, with both HFD and antibiotic treatment having a strong effect on the bacterial structure, with lesser but clear differences among strains. At the phylum level, the relative abundance of Firmicutes to Bacteroidetes was higher in both chow-fed 129 strains compared to B6J mice. HFD feeding reduced Bacteroidetes in all strains of mice. Both antibiotics resulted in elimination of most of the bacteria, except for Firmicutes in B6J and 129J mice, whereas, in 129T mice, considerable Proteobacteria and Verrucomicrobia remained. |
|
Formal Description Interaction-ID: 89072 |
environment high-fat diet decreases_quantity of environment Bacteroidetes |
| Comment | A high-fat diet markedly increased the levels of multiple bile acids in the cecum in all strains of mice, and this was largely reversed by treatment with either vancomycin or metronidazole. In the plasma, chow and HFD mice had similar levels of most bile acids, but antibiotic treatment did lower the levels of the secondary bile acid taurodeoxycholic acid, reflecting the change in the cecum. |
|
Formal Description Interaction-ID: 89073 |
|
| Comment | A high-fat diet markedly increased the levels of multiple bile acids in the cecum in all strains of mice, and this was largely reversed by treatment with either vancomycin or metronidazole. In the plasma, chow and HFD mice had similar levels of most bile acids, but antibiotic treatment did lower the levels of the secondary bile acid taurodeoxycholic acid, reflecting the change in the cecum. |
|
Formal Description Interaction-ID: 89080 |
|
| Comment | A high-fat diet markedly increased the levels of multiple bile acids in the cecum in all strains of mice, and this was largely reversed by treatment with either vancomycin or metronidazole. In the plasma, chow and HFD mice had similar levels of most bile acids, but antibiotic treatment did lower the levels of the secondary bile acid taurodeoxycholic acid, reflecting the change in the cecum. |
|
Formal Description Interaction-ID: 89081 |
environment high-fat diet NOT affects_quantity of drug/chemical compound |
| Comment | A high-fat diet markedly increased the levels of multiple bile acids in the cecum in all strains of mice, and this was largely reversed by treatment with either vancomycin or metronidazole. In the plasma, chow and HFD mice had similar levels of most bile acids, but antibiotic treatment did lower the levels of the secondary bile acid taurodeoxycholic acid, reflecting the change in the cecum. |
|
Formal Description Interaction-ID: 89082 |
environment antibiotic intake decreases_quantity of drug/chemical compound |
| Comment | One of the most dramatically changed classes of lipids was the acylcarnitines. In the cecum, virtually all acylcarnitines, especially short-chain (C5-C9) acylcarnitines, showed modest increases on HFD and even more dramatic increases following antibiotic therapy, indicating effects of the changing microbiome on lipid metabolism in the gut. By contrast, in the plasma, the short-chain acylcarnitines decreased on an HFD, and there was little effect of antibiotics. |
|
Formal Description Interaction-ID: 89084 |
environment high-fat diet increases_quantity of drug/chemical compound Fatty acid acylcarnitine |
| Comment | One of the most dramatically changed classes of lipids was the acylcarnitines. In the cecum, virtually all acylcarnitines, especially short-chain (C5-C9) acylcarnitines, showed modest increases on HFD and even more dramatic increases following antibiotic therapy, indicating effects of the changing microbiome on lipid metabolism in the gut. By contrast, in the plasma, the short-chain acylcarnitines decreased on an HFD, and there was little effect of antibiotics. |
|
Formal Description Interaction-ID: 89087 |
environment antibiotic intake increases_quantity of drug/chemical compound Fatty acid acylcarnitine |
| Comment | One of the most dramatically changed classes of lipids was the acylcarnitines. In the cecum, virtually all acylcarnitines, especially short-chain (C5-C9) acylcarnitines, showed modest increases on HFD and even more dramatic increases following antibiotic therapy, indicating effects of the changing microbiome on lipid metabolism in the gut. By contrast, in the plasma, the short-chain acylcarnitines decreased on an HFD, and there was little effect of antibiotics. |
|
Formal Description Interaction-ID: 89088 |
environment high-fat diet decreases_quantity of drug/chemical compound Fatty acid acylcarnitine |
| Comment | One of the most dramatically changed classes of lipids was the acylcarnitines. In the cecum, virtually all acylcarnitines, especially short-chain (C5-C9) acylcarnitines, showed modest increases on HFD and even more dramatic increases following antibiotic therapy, indicating effects of the changing microbiome on lipid metabolism in the gut. By contrast, in the plasma, the short-chain acylcarnitines decreased on an HFD, and there was little effect of antibiotics. |
|
Formal Description Interaction-ID: 89089 |
environment antibiotic intake NOT affects_quantity of drug/chemical compound Fatty acid acylcarnitine |
| Comment | Some changes depended on the strain or breeding site of the mouse and the resulting differences in bacterial composition. For example, both antibiotics elevated allantoin in the cecum but had a reverse effect in the plasma uniquely in Jax-bred mice. Likewise, both B6J and 129J mice showed a marked decrease in cecal gamma-aminobutyric acid (GABA) levels in response to vancomycin and an increase by metronidazole, which was not seen in 129T mice. Both B6J and 129J mice also showed an increase in cecal threonine by vancomycin and a decrease by metronidazole, which was not observed in 129T mice. On the other hand, antibiotic treatment of HFD-fed mice produced a decrease in asparagine in only 129T Tac-derived mice. None of the latter changes were observed in the plasma, suggesting that gut bacterial metabolism is not the primary driver controlling the plasma levels of these metabolites. Hexose (fructose/glucose/galactose) levels in the cecum were decreased by an HFD and partially rescued by vancomycin in B6J and 129J mice but not in 129T mice; however, smaller changes were observed in plasma levels. |
|
Formal Description Interaction-ID: 89090 |
environment antibiotic intake affects_quantity of drug/chemical compound |
| Comment | Some changes depended on the strain or breeding site of the mouse and the resulting differences in bacterial composition. For example, both antibiotics elevated allantoin in the cecum but had a reverse effect in the plasma uniquely in Jax-bred mice. Likewise, both B6J and 129J mice showed a marked decrease in cecal gamma-aminobutyric acid (GABA) levels in response to vancomycin and an increase by metronidazole, which was not seen in 129T mice. Both B6J and 129J mice also showed an increase in cecal threonine by vancomycin and a decrease by metronidazole, which was not observed in 129T mice. On the other hand, antibiotic treatment of HFD-fed mice produced a decrease in asparagine in only 129T Tac-derived mice. None of the latter changes were observed in the plasma, suggesting that gut bacterial metabolism is not the primary driver controlling the plasma levels of these metabolites. Hexose (fructose/glucose/galactose) levels in the cecum were decreased by an HFD and partially rescued by vancomycin in B6J and 129J mice but not in 129T mice; however, smaller changes were observed in plasma levels. |
|
Formal Description Interaction-ID: 89091 |
environment antibiotic intake affects_quantity of drug/chemical compound |
| Comment | Some changes depended on the strain or breeding site of the mouse and the resulting differences in bacterial composition. For example, both antibiotics elevated allantoin in the cecum but had a reverse effect in the plasma uniquely in Jax-bred mice. Likewise, both B6J and 129J mice showed a marked decrease in cecal gamma-aminobutyric acid (GABA) levels in response to vancomycin and an increase by metronidazole, which was not seen in 129T mice. Both B6J and 129J mice also showed an increase in cecal threonine by vancomycin and a decrease by metronidazole, which was not observed in 129T mice. On the other hand, antibiotic treatment of HFD-fed mice produced a decrease in asparagine in only 129T Tac-derived mice. None of the latter changes were observed in the plasma, suggesting that gut bacterial metabolism is not the primary driver controlling the plasma levels of these metabolites. Hexose (fructose/glucose/galactose) levels in the cecum were decreased by an HFD and partially rescued by vancomycin in B6J and 129J mice but not in 129T mice; however, smaller changes were observed in plasma levels. |
|
Formal Description Interaction-ID: 89092 |
environment antibiotic intake affects_quantity of drug/chemical compound |
| Comment | Some changes depended on the strain or breeding site of the mouse and the resulting differences in bacterial composition. For example, both antibiotics elevated allantoin in the cecum but had a reverse effect in the plasma uniquely in Jax-bred mice. Likewise, both B6J and 129J mice showed a marked decrease in cecal gamma-aminobutyric acid (GABA) levels in response to vancomycin and an increase by metronidazole, which was not seen in 129T mice. Both B6J and 129J mice also showed an increase in cecal threonine by vancomycin and a decrease by metronidazole, which was not observed in 129T mice. On the other hand, antibiotic treatment of HFD-fed mice produced a decrease in asparagine in only 129T Tac-derived mice. None of the latter changes were observed in the plasma, suggesting that gut bacterial metabolism is not the primary driver controlling the plasma levels of these metabolites. Hexose (fructose/glucose/galactose) levels in the cecum were decreased by an HFD and partially rescued by vancomycin in B6J and 129J mice but not in 129T mice; however, smaller changes were observed in plasma levels. |
|
Formal Description Interaction-ID: 89093 |
environment antibiotic intake affects_quantity of drug/chemical compound |
| Comment | Some changes depended on the strain or breeding site of the mouse and the resulting differences in bacterial composition. For example, both antibiotics elevated allantoin in the cecum but had a reverse effect in the plasma uniquely in Jax-bred mice. Likewise, both B6J and 129J mice showed a marked decrease in cecal gamma-aminobutyric acid (GABA) levels in response to vancomycin and an increase by metronidazole, which was not seen in 129T mice. Both B6J and 129J mice also showed an increase in cecal threonine by vancomycin and a decrease by metronidazole, which was not observed in 129T mice. On the other hand, antibiotic treatment of HFD-fed mice produced a decrease in asparagine in only 129T Tac-derived mice. None of the latter changes were observed in the plasma, suggesting that gut bacterial metabolism is not the primary driver controlling the plasma levels of these metabolites. Hexose (fructose/glucose/galactose) levels in the cecum were decreased by an HFD and partially rescued by vancomycin in B6J and 129J mice but not in 129T mice; however, smaller changes were observed in plasma levels. |
|
Formal Description Interaction-ID: 89094 |
environment antibiotic intake affects_quantity of drug/chemical compound |
| Comment | Compared with chow-fed mice, the levels of pyrimidine metabolites (uridine, thymidine, cytosine, and 2-deoxcytidine) in the cecum were decreased by an HFD in both Jax-derived strains, and this decrease was reversed by vancomycin treatment but potentiated by metronidazole treatment. However, the plasma levels did not reflect the cecum levels. Thus, metronidazole treatment decreased the levels of uridine in the cecum but increased the levels in the plasma. |
|
Formal Description Interaction-ID: 89095 |
|
| Drugbank entries | Show/Hide entries for |
| Comment | Compared with chow-fed mice, the levels of pyrimidine metabolites (uridine, thymidine, cytosine, and 2-deoxcytidine) in the cecum were decreased by an HFD in both Jax-derived strains, and this decrease was reversed by vancomycin treatment but potentiated by metronidazole treatment. However, the plasma levels did not reflect the cecum levels. Thus, metronidazole treatment decreased the levels of uridine in the cecum but increased the levels in the plasma. |
|
Formal Description Interaction-ID: 89096 |
|
| Comment | Compared with chow-fed mice, the levels of pyrimidine metabolites (uridine, thymidine, cytosine, and 2-deoxcytidine) in the cecum were decreased by an HFD in both Jax-derived strains, and this decrease was reversed by vancomycin treatment but potentiated by metronidazole treatment. However, the plasma levels did not reflect the cecum levels. Thus, metronidazole treatment decreased the levels of uridine in the cecum but increased the levels in the plasma. |
|
Formal Description Interaction-ID: 89097 |
|
| Comment | Compared with chow-fed mice, the levels of pyrimidine metabolites (uridine, thymidine, cytosine, and 2-deoxcytidine) in the cecum were decreased by an HFD in both Jax-derived strains, and this decrease was reversed by vancomycin treatment but potentiated by metronidazole treatment. However, the plasma levels did not reflect the cecum levels. Thus, metronidazole treatment decreased the levels of uridine in the cecum but increased the levels in the plasma. |
|
Formal Description Interaction-ID: 89098 |
|
| Comment | Compared with chow-fed mice, the levels of pyrimidine metabolites (uridine, thymidine, cytosine, and 2-deoxcytidine) in the cecum were decreased by an HFD in both Jax-derived strains, and this decrease was reversed by vancomycin treatment but potentiated by metronidazole treatment. However, the plasma levels did not reflect the cecum levels. Thus, metronidazole treatment decreased the levels of uridine in the cecum but increased the levels in the plasma. |
|
Formal Description Interaction-ID: 89099 |
|
| Drugbank entries | Show/Hide entries for |
| Comment | Compared with chow-fed mice, the levels of pyrimidine metabolites (uridine, thymidine, cytosine, and 2-deoxcytidine) in the cecum were decreased by an HFD in both Jax-derived strains, and this decrease was reversed by vancomycin treatment but potentiated by metronidazole treatment. However, the plasma levels did not reflect the cecum levels. Thus, metronidazole treatment decreased the levels of uridine in the cecum but increased the levels in the plasma. |
|
Formal Description Interaction-ID: 89100 |
|
| Comment | Compared with chow-fed mice, the levels of pyrimidine metabolites (uridine, thymidine, cytosine, and 2-deoxcytidine) in the cecum were decreased by an HFD in both Jax-derived strains, and this decrease was reversed by vancomycin treatment but potentiated by metronidazole treatment. However, the plasma levels did not reflect the cecum levels. Thus, metronidazole treatment decreased the levels of uridine in the cecum but increased the levels in the plasma. |
|
Formal Description Interaction-ID: 89101 |
|
| Comment | Compared with chow-fed mice, the levels of pyrimidine metabolites (uridine, thymidine, cytosine, and 2-deoxcytidine) in the cecum were decreased by an HFD in both Jax-derived strains, and this decrease was reversed by vancomycin treatment but potentiated by metronidazole treatment. However, the plasma levels did not reflect the cecum levels. Thus, metronidazole treatment decreased the levels of uridine in the cecum but increased the levels in the plasma. |
|
Formal Description Interaction-ID: 89102 |
|
| Comment | Compared with chow-fed mice, the levels of pyrimidine metabolites (uridine, thymidine, cytosine, and 2-deoxcytidine) in the cecum were decreased by an HFD in both Jax-derived strains, and this decrease was reversed by vancomycin treatment but potentiated by metronidazole treatment. However, the plasma levels did not reflect the cecum levels. Thus, metronidazole treatment decreased the levels of uridine in the cecum but increased the levels in the plasma. |
|
Formal Description Interaction-ID: 89103 |
|
| Drugbank entries | Show/Hide entries for |
| Comment | Compared with chow-fed mice, the levels of pyrimidine metabolites (uridine, thymidine, cytosine, and 2-deoxcytidine) in the cecum were decreased by an HFD in both Jax-derived strains, and this decrease was reversed by vancomycin treatment but potentiated by metronidazole treatment. However, the plasma levels did not reflect the cecum levels. Thus, metronidazole treatment decreased the levels of uridine in the cecum but increased the levels in the plasma. |
|
Formal Description Interaction-ID: 89104 |
|
| Comment | Compared with chow-fed mice, the levels of pyrimidine metabolites (uridine, thymidine, cytosine, and 2-deoxcytidine) in the cecum were decreased by an HFD in both Jax-derived strains, and this decrease was reversed by vancomycin treatment but potentiated by metronidazole treatment. However, the plasma levels did not reflect the cecum levels. Thus, metronidazole treatment decreased the levels of uridine in the cecum but increased the levels in the plasma. |
|
Formal Description Interaction-ID: 89105 |
|
| Comment | Compared with chow-fed mice, the levels of pyrimidine metabolites (uridine, thymidine, cytosine, and 2-deoxcytidine) in the cecum were decreased by an HFD in both Jax-derived strains, and this decrease was reversed by vancomycin treatment but potentiated by metronidazole treatment. However, the plasma levels did not reflect the cecum levels. Thus, metronidazole treatment decreased the levels of uridine in the cecum but increased the levels in the plasma. |
|
Formal Description Interaction-ID: 89106 |
environment metronidazole intake decreases_quantity of drug/chemical compound |
| Comment | Compared with chow-fed mice, the levels of pyrimidine metabolites (uridine, thymidine, cytosine, and 2-deoxcytidine) in the cecum were decreased by an HFD in both Jax-derived strains, and this decrease was reversed by vancomycin treatment but potentiated by metronidazole treatment. However, the plasma levels did not reflect the cecum levels. Thus, metronidazole treatment decreased the levels of uridine in the cecum but increased the levels in the plasma. |
|
Formal Description Interaction-ID: 89107 |
environment metronidazole intake increases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for |
| Comment | The HFD induced large decreases in cecal levels of AMP, ADP, and cytidine monophosphate (CMP) and nucleosides such as inosine. These changes were most dramatic in B6J and 129J mice and reversed by vancomycin but not metronidazole. |
|
Formal Description Interaction-ID: 89108 |
|
| Comment | The HFD induced large decreases in cecal levels of AMP, ADP, and cytidine monophosphate (CMP) and nucleosides such as inosine. These changes were most dramatic in B6J and 129J mice and reversed by vancomycin but not metronidazole. |
|
Formal Description Interaction-ID: 89109 |
|
| Comment | The HFD induced large decreases in cecal levels of AMP, ADP, and cytidine monophosphate (CMP) and nucleosides such as inosine. These changes were most dramatic in B6J and 129J mice and reversed by vancomycin but not metronidazole. |
|
Formal Description Interaction-ID: 89110 |
|
| Comment | The HFD induced large decreases in cecal levels of AMP, ADP, and cytidine monophosphate (CMP) and nucleosides such as inosine. These changes were most dramatic in B6J and 129J mice and reversed by vancomycin but not metronidazole. |
|
Formal Description Interaction-ID: 89111 |
|
| Comment | The HFD induced large decreases in cecal levels of AMP, ADP, and cytidine monophosphate (CMP) and nucleosides such as inosine. These changes were most dramatic in B6J and 129J mice and reversed by vancomycin but not metronidazole. |
|
Formal Description Interaction-ID: 89112 |
|
| Comment | The HFD induced large decreases in cecal levels of AMP, ADP, and cytidine monophosphate (CMP) and nucleosides such as inosine. These changes were most dramatic in B6J and 129J mice and reversed by vancomycin but not metronidazole. |
|
Formal Description Interaction-ID: 89113 |
|
| Comment | The HFD induced large decreases in cecal levels of AMP, ADP, and cytidine monophosphate (CMP) and nucleosides such as inosine. These changes were most dramatic in B6J and 129J mice and reversed by vancomycin but not metronidazole. |
|
Formal Description Interaction-ID: 89114 |
|
| Comment | The HFD induced large decreases in cecal levels of AMP, ADP, and cytidine monophosphate (CMP) and nucleosides such as inosine. These changes were most dramatic in B6J and 129J mice and reversed by vancomycin but not metronidazole. |
|
Formal Description Interaction-ID: 89115 |
|
| Comment | The HFD induced large decreases in cecal levels of AMP, ADP, and cytidine monophosphate (CMP) and nucleosides such as inosine. These changes were most dramatic in B6J and 129J mice and reversed by vancomycin but not metronidazole. |
|
Formal Description Interaction-ID: 89116 |
|
| Comment | The HFD induced large decreases in cecal levels of AMP, ADP, and cytidine monophosphate (CMP) and nucleosides such as inosine. These changes were most dramatic in B6J and 129J mice and reversed by vancomycin but not metronidazole. |
|
Formal Description Interaction-ID: 89117 |
|
| Comment | The HFD induced large decreases in cecal levels of AMP, ADP, and cytidine monophosphate (CMP) and nucleosides such as inosine. These changes were most dramatic in B6J and 129J mice and reversed by vancomycin but not metronidazole. |
|
Formal Description Interaction-ID: 89118 |
|
| Comment | The HFD induced large decreases in cecal levels of AMP, ADP, and cytidine monophosphate (CMP) and nucleosides such as inosine. These changes were most dramatic in B6J and 129J mice and reversed by vancomycin but not metronidazole. |
|
Formal Description Interaction-ID: 89119 |
|
| Comment | HFD significantly increased cyclic AMP (cAMP) levels in the cecum in all strains of mice, and these were further increased by vancomycin treatment. |
|
Formal Description Interaction-ID: 89120 |
|
| Drugbank entries | Show/Hide entries for cAMP |
| Comment | HFD significantly increased cyclic AMP (cAMP) levels in the cecum in all strains of mice, and these were further increased by vancomycin treatment. |
|
Formal Description Interaction-ID: 89121 |
|
| Drugbank entries | Show/Hide entries for cAMP |
| Comment | As reported previously, branched-chain amino acids (BCAAs) such as valine, leucine, and isoleucine were elevated in the plasma by an HFD. This occurred in all strains despite differences in propensity to obesity or insulin resistance and despite variable effects on cecal levels of BCAAs. The effects of antibiotics to modify this response were strain- and amino acid-dependent. Thus, vancomycin decreased all BCAAs in the cecum, especially in the two obesity-prone strains (B6J and 129T), whereas metronidazole tended to decrease the levels of leucine and isoleucine and increase the levels of valine. Interestingly, both antibiotics increased the levels of BCAAs in the plasma of all mice, despite the fact that antibiotics improved insulin sensitivity. |
|
Formal Description Interaction-ID: 89123 |
|
| Comment | As reported previously, branched-chain amino acids (BCAAs) such as valine, leucine, and isoleucine were elevated in the plasma by an HFD. This occurred in all strains despite differences in propensity to obesity or insulin resistance and despite variable effects on cecal levels of BCAAs. The effects of antibiotics to modify this response were strain- and amino acid-dependent. Thus, vancomycin decreased all BCAAs in the cecum, especially in the two obesity-prone strains (B6J and 129T), whereas metronidazole tended to decrease the levels of leucine and isoleucine and increase the levels of valine. Interestingly, both antibiotics increased the levels of BCAAs in the plasma of all mice, despite the fact that antibiotics improved insulin sensitivity. |
|
Formal Description Interaction-ID: 89137 |
|
| Comment | As reported previously, branched-chain amino acids (BCAAs) such as valine, leucine, and isoleucine were elevated in the plasma by an HFD. This occurred in all strains despite differences in propensity to obesity or insulin resistance and despite variable effects on cecal levels of BCAAs. The effects of antibiotics to modify this response were strain- and amino acid-dependent. Thus, vancomycin decreased all BCAAs in the cecum, especially in the two obesity-prone strains (B6J and 129T), whereas metronidazole tended to decrease the levels of leucine and isoleucine and increase the levels of valine. Interestingly, both antibiotics increased the levels of BCAAs in the plasma of all mice, despite the fact that antibiotics improved insulin sensitivity. |
|
Formal Description Interaction-ID: 89138 |
|
| Comment | As reported previously, branched-chain amino acids (BCAAs) such as valine, leucine, and isoleucine were elevated in the plasma by an HFD. This occurred in all strains despite differences in propensity to obesity or insulin resistance and despite variable effects on cecal levels of BCAAs. The effects of antibiotics to modify this response were strain- and amino acid-dependent. Thus, vancomycin decreased all BCAAs in the cecum, especially in the two obesity-prone strains (B6J and 129T), whereas metronidazole tended to decrease the levels of leucine and isoleucine and increase the levels of valine. Interestingly, both antibiotics increased the levels of BCAAs in the plasma of all mice, despite the fact that antibiotics improved insulin sensitivity. |
|
Formal Description Interaction-ID: 89139 |
|
| Comment | As reported previously, branched-chain amino acids (BCAAs) such as valine, leucine, and isoleucine were elevated in the plasma by an HFD. This occurred in all strains despite differences in propensity to obesity or insulin resistance and despite variable effects on cecal levels of BCAAs. The effects of antibiotics to modify this response were strain- and amino acid-dependent. Thus, vancomycin decreased all BCAAs in the cecum, especially in the two obesity-prone strains (B6J and 129T), whereas metronidazole tended to decrease the levels of leucine and isoleucine and increase the levels of valine. Interestingly, both antibiotics increased the levels of BCAAs in the plasma of all mice, despite the fact that antibiotics improved insulin sensitivity. |
|
Formal Description Interaction-ID: 89140 |
|
| Comment | As reported previously, branched-chain amino acids (BCAAs) such as valine, leucine, and isoleucine were elevated in the plasma by an HFD. This occurred in all strains despite differences in propensity to obesity or insulin resistance and despite variable effects on cecal levels of BCAAs. The effects of antibiotics to modify this response were strain- and amino acid-dependent. Thus, vancomycin decreased all BCAAs in the cecum, especially in the two obesity-prone strains (B6J and 129T), whereas metronidazole tended to decrease the levels of leucine and isoleucine and increase the levels of valine. Interestingly, both antibiotics increased the levels of BCAAs in the plasma of all mice, despite the fact that antibiotics improved insulin sensitivity. |
|
Formal Description Interaction-ID: 89141 |
|
| Comment | As reported previously, branched-chain amino acids (BCAAs) such as valine, leucine, and isoleucine were elevated in the plasma by an HFD. This occurred in all strains despite differences in propensity to obesity or insulin resistance and despite variable effects on cecal levels of BCAAs. The effects of antibiotics to modify this response were strain- and amino acid-dependent. Thus, vancomycin decreased all BCAAs in the cecum, especially in the two obesity-prone strains (B6J and 129T), whereas metronidazole tended to decrease the levels of leucine and isoleucine and increase the levels of valine. Interestingly, both antibiotics increased the levels of BCAAs in the plasma of all mice, despite the fact that antibiotics improved insulin sensitivity. |
|
Formal Description Interaction-ID: 89142 |
environment metronidazole intake increases_quantity of drug/chemical compound |
| Comment | As reported previously, branched-chain amino acids (BCAAs) such as valine, leucine, and isoleucine were elevated in the plasma by an HFD. This occurred in all strains despite differences in propensity to obesity or insulin resistance and despite variable effects on cecal levels of BCAAs. The effects of antibiotics to modify this response were strain- and amino acid-dependent. Thus, vancomycin decreased all BCAAs in the cecum, especially in the two obesity-prone strains (B6J and 129T), whereas metronidazole tended to decrease the levels of leucine and isoleucine and increase the levels of valine. Interestingly, both antibiotics increased the levels of BCAAs in the plasma of all mice, despite the fact that antibiotics improved insulin sensitivity. |
|
Formal Description Interaction-ID: 89143 |
|
| Comment | As reported previously, branched-chain amino acids (BCAAs) such as valine, leucine, and isoleucine were elevated in the plasma by an HFD. This occurred in all strains despite differences in propensity to obesity or insulin resistance and despite variable effects on cecal levels of BCAAs. The effects of antibiotics to modify this response were strain- and amino acid-dependent. Thus, vancomycin decreased all BCAAs in the cecum, especially in the two obesity-prone strains (B6J and 129T), whereas metronidazole tended to decrease the levels of leucine and isoleucine and increase the levels of valine. Interestingly, both antibiotics increased the levels of BCAAs in the plasma of all mice, despite the fact that antibiotics improved insulin sensitivity. |
|
Formal Description Interaction-ID: 89144 |
|
| Comment | As reported previously, branched-chain amino acids (BCAAs) such as valine, leucine, and isoleucine were elevated in the plasma by an HFD. This occurred in all strains despite differences in propensity to obesity or insulin resistance and despite variable effects on cecal levels of BCAAs. The effects of antibiotics to modify this response were strain- and amino acid-dependent. Thus, vancomycin decreased all BCAAs in the cecum, especially in the two obesity-prone strains (B6J and 129T), whereas metronidazole tended to decrease the levels of leucine and isoleucine and increase the levels of valine. Interestingly, both antibiotics increased the levels of BCAAs in the plasma of all mice, despite the fact that antibiotics improved insulin sensitivity. |
|
Formal Description Interaction-ID: 89145 |
|
| Comment | As reported previously, branched-chain amino acids (BCAAs) such as valine, leucine, and isoleucine were elevated in the plasma by an HFD. This occurred in all strains despite differences in propensity to obesity or insulin resistance and despite variable effects on cecal levels of BCAAs. The effects of antibiotics to modify this response were strain- and amino acid-dependent. Thus, vancomycin decreased all BCAAs in the cecum, especially in the two obesity-prone strains (B6J and 129T), whereas metronidazole tended to decrease the levels of leucine and isoleucine and increase the levels of valine. Interestingly, both antibiotics increased the levels of BCAAs in the plasma of all mice, despite the fact that antibiotics improved insulin sensitivity. |
|
Formal Description Interaction-ID: 89146 |
|
| Comment | As reported previously, branched-chain amino acids (BCAAs) such as valine, leucine, and isoleucine were elevated in the plasma by an HFD. This occurred in all strains despite differences in propensity to obesity or insulin resistance and despite variable effects on cecal levels of BCAAs. The effects of antibiotics to modify this response were strain- and amino acid-dependent. Thus, vancomycin decreased all BCAAs in the cecum, especially in the two obesity-prone strains (B6J and 129T), whereas metronidazole tended to decrease the levels of leucine and isoleucine and increase the levels of valine. Interestingly, both antibiotics increased the levels of BCAAs in the plasma of all mice, despite the fact that antibiotics improved insulin sensitivity. |
|
Formal Description Interaction-ID: 89147 |
environment vancomycin intake increases_quantity of drug/chemical compound |
| Comment | As reported previously, branched-chain amino acids (BCAAs) such as valine, leucine, and isoleucine were elevated in the plasma by an HFD. This occurred in all strains despite differences in propensity to obesity or insulin resistance and despite variable effects on cecal levels of BCAAs. The effects of antibiotics to modify this response were strain- and amino acid-dependent. Thus, vancomycin decreased all BCAAs in the cecum, especially in the two obesity-prone strains (B6J and 129T), whereas metronidazole tended to decrease the levels of leucine and isoleucine and increase the levels of valine. Interestingly, both antibiotics increased the levels of BCAAs in the plasma of all mice, despite the fact that antibiotics improved insulin sensitivity. |
|
Formal Description Interaction-ID: 89148 |
environment metronidazole intake increases_quantity of drug/chemical compound |
| Comment | As reported previously, branched-chain amino acids (BCAAs) such as valine, leucine, and isoleucine were elevated in the plasma by an HFD. This occurred in all strains despite differences in propensity to obesity or insulin resistance and despite variable effects on cecal levels of BCAAs. The effects of antibiotics to modify this response were strain- and amino acid-dependent. Thus, vancomycin decreased all BCAAs in the cecum, especially in the two obesity-prone strains (B6J and 129T), whereas metronidazole tended to decrease the levels of leucine and isoleucine and increase the levels of valine. Interestingly, both antibiotics increased the levels of BCAAs in the plasma of all mice, despite the fact that antibiotics improved insulin sensitivity. |
|
Formal Description Interaction-ID: 89149 |
environment metronidazole intake increases_quantity of drug/chemical compound |
| Comment | With regard to aromatic amino acids, metronidazole treatment resulted in big decreases in phenylalanine, tyrosine, and tryptophan in the cecum of all mouse strains. Despite the changes in the cecum, the levels of these metabolites in the plasma were elevated by metronidazole, suggesting that metronidazole may have additional effects on the absorption or turnover of these metabolites. |
|
Formal Description Interaction-ID: 89150 |
environment metronidazole intake decreases_quantity of drug/chemical compound |
| Comment | With regard to aromatic amino acids, metronidazole treatment resulted in big decreases in phenylalanine, tyrosine, and tryptophan in the cecum of all mouse strains. Despite the changes in the cecum, the levels of these metabolites in the plasma were elevated by metronidazole, suggesting that metronidazole may have additional effects on the absorption or turnover of these metabolites. |
|
Formal Description Interaction-ID: 89151 |
|
| Comment | With regard to aromatic amino acids, metronidazole treatment resulted in big decreases in phenylalanine, tyrosine, and tryptophan in the cecum of all mouse strains. Despite the changes in the cecum, the levels of these metabolites in the plasma were elevated by metronidazole, suggesting that metronidazole may have additional effects on the absorption or turnover of these metabolites. |
|
Formal Description Interaction-ID: 89152 |
|
| Comment | With regard to aromatic amino acids, metronidazole treatment resulted in big decreases in phenylalanine, tyrosine, and tryptophan in the cecum of all mouse strains. Despite the changes in the cecum, the levels of these metabolites in the plasma were elevated by metronidazole, suggesting that metronidazole may have additional effects on the absorption or turnover of these metabolites. |
|
Formal Description Interaction-ID: 89153 |
environment metronidazole intake increases_quantity of drug/chemical compound |
| Comment | With regard to aromatic amino acids, metronidazole treatment resulted in big decreases in phenylalanine, tyrosine, and tryptophan in the cecum of all mouse strains. Despite the changes in the cecum, the levels of these metabolites in the plasma were elevated by metronidazole, suggesting that metronidazole may have additional effects on the absorption or turnover of these metabolites. |
|
Formal Description Interaction-ID: 89154 |
environment metronidazole intake increases_quantity of drug/chemical compound |
| Comment | With regard to aromatic amino acids, metronidazole treatment resulted in big decreases in phenylalanine, tyrosine, and tryptophan in the cecum of all mouse strains. Despite the changes in the cecum, the levels of these metabolites in the plasma were elevated by metronidazole, suggesting that metronidazole may have additional effects on the absorption or turnover of these metabolites. |
|
Formal Description Interaction-ID: 89155 |
environment metronidazole intake increases_quantity of drug/chemical compound |
| Comment | Fatty acids can have pro- or anti-inflammatory effects. An HFD had almost no effect on the levels of saturated fatty acids in the cecum, despite deriving 60% of calories from fat, mostly lard. An HFD accompanied by either antibiotic, but especially metronidazole, resulted in increased cecal levels of stearic acid (C18) but decreasing levels of palmitic (C16) and myristic acids (C14). In the plasma, a high-fat diet alone increased the levels of stearic acid in all strains, and this was not modified by antibiotic treatment. Ingestion of an HFD had variable effects on many of the unsaturated and short-chain fatty acids found in the cecum, but, except for adrenic acid (C24:4), these were largely unchanged by antibiotic treatment. In the plasma, an HFD was associated with a major decrease in eicosopentanoic acid; this closely mirrored the changes in the cecum. By contrast, an HFD increased the plasma levels of adrenic acid independent of cecal content. The plasma levels of these unsaturated fatty acids were not influenced by antibiotic treatment. Overall, the changes in plasma fatty acid levels on an HFD reflected an increase in proinflammatory fatty acids, such as adrenic and stearic acid, and a decrease in anti-inflammatory fatty acids, such as eicosopentaenoic and docosohexanoic acids. Antibiotic administration had little effect on these changes in free fatty acids in B6J mice despite improving insulin sensitivity, and the changes in free fatty acid (FFA) were similar in the insulin-sensitive 129 substrains, thus disconnecting the FFA levels from the level of insulin resistance. |
|
Formal Description Interaction-ID: 89156 |
environment high-fat diet NOT affects_quantity of drug/chemical compound Saturated fatty acid |
| Comment | Fatty acids can have pro- or anti-inflammatory effects. An HFD had almost no effect on the levels of saturated fatty acids in the cecum, despite deriving 60% of calories from fat, mostly lard. An HFD accompanied by either antibiotic, but especially metronidazole, resulted in increased cecal levels of stearic acid (C18) but decreasing levels of palmitic (C16) and myristic acids (C14). In the plasma, a high-fat diet alone increased the levels of stearic acid in all strains, and this was not modified by antibiotic treatment. Ingestion of an HFD had variable effects on many of the unsaturated and short-chain fatty acids found in the cecum, but, except for adrenic acid (C24:4), these were largely unchanged by antibiotic treatment. In the plasma, an HFD was associated with a major decrease in eicosopentanoic acid; this closely mirrored the changes in the cecum. By contrast, an HFD increased the plasma levels of adrenic acid independent of cecal content. The plasma levels of these unsaturated fatty acids were not influenced by antibiotic treatment. Overall, the changes in plasma fatty acid levels on an HFD reflected an increase in proinflammatory fatty acids, such as adrenic and stearic acid, and a decrease in anti-inflammatory fatty acids, such as eicosopentaenoic and docosohexanoic acids. Antibiotic administration had little effect on these changes in free fatty acids in B6J mice despite improving insulin sensitivity, and the changes in free fatty acid (FFA) were similar in the insulin-sensitive 129 substrains, thus disconnecting the FFA levels from the level of insulin resistance. |
|
Formal Description Interaction-ID: 89157 |
|
| Drugbank entries | Show/Hide entries for |
| Comment | Fatty acids can have pro- or anti-inflammatory effects. An HFD had almost no effect on the levels of saturated fatty acids in the cecum, despite deriving 60% of calories from fat, mostly lard. An HFD accompanied by either antibiotic, but especially metronidazole, resulted in increased cecal levels of stearic acid (C18) but decreasing levels of palmitic (C16) and myristic acids (C14). In the plasma, a high-fat diet alone increased the levels of stearic acid in all strains, and this was not modified by antibiotic treatment. Ingestion of an HFD had variable effects on many of the unsaturated and short-chain fatty acids found in the cecum, but, except for adrenic acid (C24:4), these were largely unchanged by antibiotic treatment. In the plasma, an HFD was associated with a major decrease in eicosopentanoic acid; this closely mirrored the changes in the cecum. By contrast, an HFD increased the plasma levels of adrenic acid independent of cecal content. The plasma levels of these unsaturated fatty acids were not influenced by antibiotic treatment. Overall, the changes in plasma fatty acid levels on an HFD reflected an increase in proinflammatory fatty acids, such as adrenic and stearic acid, and a decrease in anti-inflammatory fatty acids, such as eicosopentaenoic and docosohexanoic acids. Antibiotic administration had little effect on these changes in free fatty acids in B6J mice despite improving insulin sensitivity, and the changes in free fatty acid (FFA) were similar in the insulin-sensitive 129 substrains, thus disconnecting the FFA levels from the level of insulin resistance. |
|
Formal Description Interaction-ID: 89158 |
environment metronidazole intake decreases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for |
| Comment | Fatty acids can have pro- or anti-inflammatory effects. An HFD had almost no effect on the levels of saturated fatty acids in the cecum, despite deriving 60% of calories from fat, mostly lard. An HFD accompanied by either antibiotic, but especially metronidazole, resulted in increased cecal levels of stearic acid (C18) but decreasing levels of palmitic (C16) and myristic acids (C14). In the plasma, a high-fat diet alone increased the levels of stearic acid in all strains, and this was not modified by antibiotic treatment. Ingestion of an HFD had variable effects on many of the unsaturated and short-chain fatty acids found in the cecum, but, except for adrenic acid (C24:4), these were largely unchanged by antibiotic treatment. In the plasma, an HFD was associated with a major decrease in eicosopentanoic acid; this closely mirrored the changes in the cecum. By contrast, an HFD increased the plasma levels of adrenic acid independent of cecal content. The plasma levels of these unsaturated fatty acids were not influenced by antibiotic treatment. Overall, the changes in plasma fatty acid levels on an HFD reflected an increase in proinflammatory fatty acids, such as adrenic and stearic acid, and a decrease in anti-inflammatory fatty acids, such as eicosopentaenoic and docosohexanoic acids. Antibiotic administration had little effect on these changes in free fatty acids in B6J mice despite improving insulin sensitivity, and the changes in free fatty acid (FFA) were similar in the insulin-sensitive 129 substrains, thus disconnecting the FFA levels from the level of insulin resistance. |
|
Formal Description Interaction-ID: 89159 |
environment metronidazole intake decreases_quantity of drug/chemical compound |
| Drugbank entries | Show/Hide entries for |
| Comment | Fatty acids can have pro- or anti-inflammatory effects. An HFD had almost no effect on the levels of saturated fatty acids in the cecum, despite deriving 60% of calories from fat, mostly lard. An HFD accompanied by either antibiotic, but especially metronidazole, resulted in increased cecal levels of stearic acid (C18) but decreasing levels of palmitic (C16) and myristic acids (C14). In the plasma, a high-fat diet alone increased the levels of stearic acid in all strains, and this was not modified by antibiotic treatment. Ingestion of an HFD had variable effects on many of the unsaturated and short-chain fatty acids found in the cecum, but, except for adrenic acid (C24:4), these were largely unchanged by antibiotic treatment. In the plasma, an HFD was associated with a major decrease in eicosopentanoic acid; this closely mirrored the changes in the cecum. By contrast, an HFD increased the plasma levels of adrenic acid independent of cecal content. The plasma levels of these unsaturated fatty acids were not influenced by antibiotic treatment. Overall, the changes in plasma fatty acid levels on an HFD reflected an increase in proinflammatory fatty acids, such as adrenic and stearic acid, and a decrease in anti-inflammatory fatty acids, such as eicosopentaenoic and docosohexanoic acids. Antibiotic administration had little effect on these changes in free fatty acids in B6J mice despite improving insulin sensitivity, and the changes in free fatty acid (FFA) were similar in the insulin-sensitive 129 substrains, thus disconnecting the FFA levels from the level of insulin resistance. |
|
Formal Description Interaction-ID: 89160 |
|
| Drugbank entries | Show/Hide entries for |
| Comment | Fatty acids can have pro- or anti-inflammatory effects. An HFD had almost no effect on the levels of saturated fatty acids in the cecum, despite deriving 60% of calories from fat, mostly lard. An HFD accompanied by either antibiotic, but especially metronidazole, resulted in increased cecal levels of stearic acid (C18) but decreasing levels of palmitic (C16) and myristic acids (C14). In the plasma, a high-fat diet alone increased the levels of stearic acid in all strains, and this was not modified by antibiotic treatment. Ingestion of an HFD had variable effects on many of the unsaturated and short-chain fatty acids found in the cecum, but, except for adrenic acid (C24:4), these were largely unchanged by antibiotic treatment. In the plasma, an HFD was associated with a major decrease in eicosopentanoic acid; this closely mirrored the changes in the cecum. By contrast, an HFD increased the plasma levels of adrenic acid independent of cecal content. The plasma levels of these unsaturated fatty acids were not influenced by antibiotic treatment. Overall, the changes in plasma fatty acid levels on an HFD reflected an increase in proinflammatory fatty acids, such as adrenic and stearic acid, and a decrease in anti-inflammatory fatty acids, such as eicosopentaenoic and docosohexanoic acids. Antibiotic administration had little effect on these changes in free fatty acids in B6J mice despite improving insulin sensitivity, and the changes in free fatty acid (FFA) were similar in the insulin-sensitive 129 substrains, thus disconnecting the FFA levels from the level of insulin resistance. |
|
Formal Description Interaction-ID: 89161 |
|
| Comment | Fatty acids can have pro- or anti-inflammatory effects. An HFD had almost no effect on the levels of saturated fatty acids in the cecum, despite deriving 60% of calories from fat, mostly lard. An HFD accompanied by either antibiotic, but especially metronidazole, resulted in increased cecal levels of stearic acid (C18) but decreasing levels of palmitic (C16) and myristic acids (C14). In the plasma, a high-fat diet alone increased the levels of stearic acid in all strains, and this was not modified by antibiotic treatment. Ingestion of an HFD had variable effects on many of the unsaturated and short-chain fatty acids found in the cecum, but, except for adrenic acid (C24:4), these were largely unchanged by antibiotic treatment. In the plasma, an HFD was associated with a major decrease in eicosopentanoic acid; this closely mirrored the changes in the cecum. By contrast, an HFD increased the plasma levels of adrenic acid independent of cecal content. The plasma levels of these unsaturated fatty acids were not influenced by antibiotic treatment. Overall, the changes in plasma fatty acid levels on an HFD reflected an increase in proinflammatory fatty acids, such as adrenic and stearic acid, and a decrease in anti-inflammatory fatty acids, such as eicosopentaenoic and docosohexanoic acids. Antibiotic administration had little effect on these changes in free fatty acids in B6J mice despite improving insulin sensitivity, and the changes in free fatty acid (FFA) were similar in the insulin-sensitive 129 substrains, thus disconnecting the FFA levels from the level of insulin resistance. |
|
Formal Description Interaction-ID: 89162 |
environment high-fat diet decreases_quantity of drug/chemical compound |
| Comment | Fatty acids can have pro- or anti-inflammatory effects. An HFD had almost no effect on the levels of saturated fatty acids in the cecum, despite deriving 60% of calories from fat, mostly lard. An HFD accompanied by either antibiotic, but especially metronidazole, resulted in increased cecal levels of stearic acid (C18) but decreasing levels of palmitic (C16) and myristic acids (C14). In the plasma, a high-fat diet alone increased the levels of stearic acid in all strains, and this was not modified by antibiotic treatment. Ingestion of an HFD had variable effects on many of the unsaturated and short-chain fatty acids found in the cecum, but, except for adrenic acid (C24:4), these were largely unchanged by antibiotic treatment. In the plasma, an HFD was associated with a major decrease in eicosopentanoic acid; this closely mirrored the changes in the cecum. By contrast, an HFD increased the plasma levels of adrenic acid independent of cecal content. The plasma levels of these unsaturated fatty acids were not influenced by antibiotic treatment. Overall, the changes in plasma fatty acid levels on an HFD reflected an increase in proinflammatory fatty acids, such as adrenic and stearic acid, and a decrease in anti-inflammatory fatty acids, such as eicosopentaenoic and docosohexanoic acids. Antibiotic administration had little effect on these changes in free fatty acids in B6J mice despite improving insulin sensitivity, and the changes in free fatty acid (FFA) were similar in the insulin-sensitive 129 substrains, thus disconnecting the FFA levels from the level of insulin resistance. |
|
Formal Description Interaction-ID: 89163 |
|
| Comment | The plasma levels of metabolites also showed a dynamic variation in response to strain, diet, and antibiotics, even for metabolites that were not changed or not changed in the same direction in the cecum. For example, short-chain fatty acids are well-known bacterial metabolites, but propionate levels were unchanged in the cecum of any strain by HFD alone, but the HFD increased propionate in the plasma of B6J mice. Both antibiotics decreased propionate in the cecum and plasma in B6J mice but had variable effects in 129 mice, indicating differences dependent on genetic background, the site (vendor) where the mice were born, as well as diet and antibiotic treatment. The plasma levels of C34:3 phosphatidylethanolamine (PE) plasmalogen and C5-carnitine were 4-fold higher in both strains of 129 mice compared with B6J mice under all conditions, whereas C30:0 PC was higher in B6J compared with 129 mice, indicating that genetic background/strain is an important factor affecting plasma metabolite levels. |
|
Formal Description Interaction-ID: 89164 |
|
| Comment | The plasma levels of metabolites also showed a dynamic variation in response to strain, diet, and antibiotics, even for metabolites that were not changed or not changed in the same direction in the cecum. For example, short-chain fatty acids are well-known bacterial metabolites, but propionate levels were unchanged in the cecum of any strain by HFD alone, but the HFD increased propionate in the plasma of B6J mice. Both antibiotics decreased propionate in the cecum and plasma in B6J mice but had variable effects in 129 mice, indicating differences dependent on genetic background, the site (vendor) where the mice were born, as well as diet and antibiotic treatment. The plasma levels of C34:3 phosphatidylethanolamine (PE) plasmalogen and C5-carnitine were 4-fold higher in both strains of 129 mice compared with B6J mice under all conditions, whereas C30:0 PC was higher in B6J compared with 129 mice, indicating that genetic background/strain is an important factor affecting plasma metabolite levels. |
|
Formal Description Interaction-ID: 89165 |
environment high-fat diet increases_quantity of drug/chemical compound |
| Comment | The plasma levels of metabolites also showed a dynamic variation in response to strain, diet, and antibiotics, even for metabolites that were not changed or not changed in the same direction in the cecum. For example, short-chain fatty acids are well-known bacterial metabolites, but propionate levels were unchanged in the cecum of any strain by HFD alone, but the HFD increased propionate in the plasma of B6J mice. Both antibiotics decreased propionate in the cecum and plasma in B6J mice but had variable effects in 129 mice, indicating differences dependent on genetic background, the site (vendor) where the mice were born, as well as diet and antibiotic treatment. The plasma levels of C34:3 phosphatidylethanolamine (PE) plasmalogen and C5-carnitine were 4-fold higher in both strains of 129 mice compared with B6J mice under all conditions, whereas C30:0 PC was higher in B6J compared with 129 mice, indicating that genetic background/strain is an important factor affecting plasma metabolite levels. |
|
Formal Description Interaction-ID: 89166 |
environment antibiotic intake decreases_quantity of drug/chemical compound |
| Comment | Other plasma metabolites were mildly or not affected by diet but dramatically affected by antibiotics, indicating that they are likely direct or indirect products of intestinal bacterial metabolism. For example, indoxylsulfate, a bacterial metabolite that acts as a uremic toxin, was increased in the cecum of all three strains by both antibiotics, whereas plasma levels in B6J but not 129 mice decreased with antibiotics. Both plasma and cecal levels of phenylacetylglycine were decreased about 4- to 8-fold by both antibiotics in all strains. In contrast, the plasma levels of trimethylamine-N-oxide, another bacterial metabolite that has been linked to cardiovascular disease risk, were markedly decreased by vancomycin, but not metronidazole, in B6J and 129J mice, whereas cecal levels showed no consistent pattern. |
|
Formal Description Interaction-ID: 89167 |
environment antibiotic intake increases_quantity of drug/chemical compound Indoxyl sulfate |
| Comment | Other plasma metabolites were mildly or not affected by diet but dramatically affected by antibiotics, indicating that they are likely direct or indirect products of intestinal bacterial metabolism. For example, indoxylsulfate, a bacterial metabolite that acts as a uremic toxin, was increased in the cecum of all three strains by both antibiotics, whereas plasma levels in B6J but not 129 mice decreased with antibiotics. Both plasma and cecal levels of phenylacetylglycine were decreased about 4- to 8-fold by both antibiotics in all strains. In contrast, the plasma levels of trimethylamine-N-oxide, another bacterial metabolite that has been linked to cardiovascular disease risk, were markedly decreased by vancomycin, but not metronidazole, in B6J and 129J mice, whereas cecal levels showed no consistent pattern. |
|
Formal Description Interaction-ID: 89168 |
environment antibiotic intake decreases_quantity of drug/chemical compound |
| Comment | Other plasma metabolites were mildly or not affected by diet but dramatically affected by antibiotics, indicating that they are likely direct or indirect products of intestinal bacterial metabolism. For example, indoxylsulfate, a bacterial metabolite that acts as a uremic toxin, was increased in the cecum of all three strains by both antibiotics, whereas plasma levels in B6J but not 129 mice decreased with antibiotics. Both plasma and cecal levels of phenylacetylglycine were decreased about 4- to 8-fold by both antibiotics in all strains. In contrast, the plasma levels of trimethylamine-N-oxide, another bacterial metabolite that has been linked to cardiovascular disease risk, were markedly decreased by vancomycin, but not metronidazole, in B6J and 129J mice, whereas cecal levels showed no consistent pattern. |
|
Formal Description Interaction-ID: 89169 |
environment vancomycin intake decreases_quantity of drug/chemical compound |
| Comment | Other plasma metabolites were mildly or not affected by diet but dramatically affected by antibiotics, indicating that they are likely direct or indirect products of intestinal bacterial metabolism. For example, indoxylsulfate, a bacterial metabolite that acts as a uremic toxin, was increased in the cecum of all three strains by both antibiotics, whereas plasma levels in B6J but not 129 mice decreased with antibiotics. Both plasma and cecal levels of phenylacetylglycine were decreased about 4- to 8-fold by both antibiotics in all strains. In contrast, the plasma levels of trimethylamine-N-oxide, another bacterial metabolite that has been linked to cardiovascular disease risk, were markedly decreased by vancomycin, but not metronidazole, in B6J and 129J mice, whereas cecal levels showed no consistent pattern. |
|
Formal Description Interaction-ID: 89170 |
environment metronidazole intake NOT affects_quantity of drug/chemical compound |
| Comment | In the cecum, histidine levels were not affected by an HFD, but in mice from Jax (B6J and 129J), histidine was increased by vancomycin and decreased by metronidazole treatment. By contrast, in 129T mice, histidine was decreased by both antibiotics. L-histamine, N-acetyl-histamine, histadinal, histadinol, 1-methyl-histamine, and anserine in the cecum were all decreased by an HFD and not rescued by either antibiotic. Of these, only L-histamine and anserine can be made in mammalian cells and were found in the plasma, and both tended to go up, not down. However, N-acetylhistamine showed identical patterns in the plasma and cecum, suggesting that the levels of this metabolite in the plasma are purely derived from gut microbial metabolism. |
|
Formal Description Interaction-ID: 89171 |
|
| Comment | In the cecum, histidine levels were not affected by an HFD, but in mice from Jax (B6J and 129J), histidine was increased by vancomycin and decreased by metronidazole treatment. By contrast, in 129T mice, histidine was decreased by both antibiotics. L-histamine, N-acetyl-histamine, histadinal, histadinol, 1-methyl-histamine, and anserine in the cecum were all decreased by an HFD and not rescued by either antibiotic. Of these, only L-histamine and anserine can be made in mammalian cells and were found in the plasma, and both tended to go up, not down. However, N-acetylhistamine showed identical patterns in the plasma and cecum, suggesting that the levels of this metabolite in the plasma are purely derived from gut microbial metabolism. |
|
Formal Description Interaction-ID: 89174 |
environment vancomycin intake increases_quantity of drug/chemical compound |
| Comment | In the cecum, histidine levels were not affected by an HFD, but in mice from Jax (B6J and 129J), histidine was increased by vancomycin and decreased by metronidazole treatment. By contrast, in 129T mice, histidine was decreased by both antibiotics. L-histamine, N-acetyl-histamine, histadinal, histadinol, 1-methyl-histamine, and anserine in the cecum were all decreased by an HFD and not rescued by either antibiotic. Of these, only L-histamine and anserine can be made in mammalian cells and were found in the plasma, and both tended to go up, not down. However, N-acetylhistamine showed identical patterns in the plasma and cecum, suggesting that the levels of this metabolite in the plasma are purely derived from gut microbial metabolism. |
|
Formal Description Interaction-ID: 89175 |
environment metronidazole intake decreases_quantity of drug/chemical compound |
| Comment | In the cecum, histidine levels were not affected by an HFD, but in mice from Jax (B6J and 129J), histidine was increased by vancomycin and decreased by metronidazole treatment. By contrast, in 129T mice, histidine was decreased by both antibiotics. L-histamine, N-acetyl-histamine, histadinal, histadinol, 1-methyl-histamine, and anserine in the cecum were all decreased by an HFD and not rescued by either antibiotic. Of these, only L-histamine and anserine can be made in mammalian cells and were found in the plasma, and both tended to go up, not down. However, N-acetylhistamine showed identical patterns in the plasma and cecum, suggesting that the levels of this metabolite in the plasma are purely derived from gut microbial metabolism. |
|
Formal Description Interaction-ID: 89176 |
environment vancomycin intake decreases_quantity of drug/chemical compound |
| Comment | In the cecum, histidine levels were not affected by an HFD, but in mice from Jax (B6J and 129J), histidine was increased by vancomycin and decreased by metronidazole treatment. By contrast, in 129T mice, histidine was decreased by both antibiotics. L-histamine, N-acetyl-histamine, histadinal, histadinol, 1-methyl-histamine, and anserine in the cecum were all decreased by an HFD and not rescued by either antibiotic. Of these, only L-histamine and anserine can be made in mammalian cells and were found in the plasma, and both tended to go up, not down. However, N-acetylhistamine showed identical patterns in the plasma and cecum, suggesting that the levels of this metabolite in the plasma are purely derived from gut microbial metabolism. |
|
Formal Description Interaction-ID: 89177 |
|
| Comment | In the cecum, histidine levels were not affected by an HFD, but in mice from Jax (B6J and 129J), histidine was increased by vancomycin and decreased by metronidazole treatment. By contrast, in 129T mice, histidine was decreased by both antibiotics. L-histamine, N-acetyl-histamine, histadinal, histadinol, 1-methyl-histamine, and anserine in the cecum were all decreased by an HFD and not rescued by either antibiotic. Of these, only L-histamine and anserine can be made in mammalian cells and were found in the plasma, and both tended to go up, not down. However, N-acetylhistamine showed identical patterns in the plasma and cecum, suggesting that the levels of this metabolite in the plasma are purely derived from gut microbial metabolism. |
|
Formal Description Interaction-ID: 89178 |
|
| Drugbank entries | Show/Hide entries for |
| Comment | In the cecum, histidine levels were not affected by an HFD, but in mice from Jax (B6J and 129J), histidine was increased by vancomycin and decreased by metronidazole treatment. By contrast, in 129T mice, histidine was decreased by both antibiotics. L-histamine, N-acetyl-histamine, histadinal, histadinol, 1-methyl-histamine, and anserine in the cecum were all decreased by an HFD and not rescued by either antibiotic. Of these, only L-histamine and anserine can be made in mammalian cells and were found in the plasma, and both tended to go up, not down. However, N-acetylhistamine showed identical patterns in the plasma and cecum, suggesting that the levels of this metabolite in the plasma are purely derived from gut microbial metabolism. |
|
Formal Description Interaction-ID: 89179 |
environment high-fat diet decreases_quantity of drug/chemical compound Histidinal |
| Comment | In the cecum, histidine levels were not affected by an HFD, but in mice from Jax (B6J and 129J), histidine was increased by vancomycin and decreased by metronidazole treatment. By contrast, in 129T mice, histidine was decreased by both antibiotics. L-histamine, N-acetyl-histamine, histadinal, histadinol, 1-methyl-histamine, and anserine in the cecum were all decreased by an HFD and not rescued by either antibiotic. Of these, only L-histamine and anserine can be made in mammalian cells and were found in the plasma, and both tended to go up, not down. However, N-acetylhistamine showed identical patterns in the plasma and cecum, suggesting that the levels of this metabolite in the plasma are purely derived from gut microbial metabolism. |
|
Formal Description Interaction-ID: 89181 |
environment high-fat diet decreases_quantity of drug/chemical compound Histadinol |
| Comment | In the cecum, histidine levels were not affected by an HFD, but in mice from Jax (B6J and 129J), histidine was increased by vancomycin and decreased by metronidazole treatment. By contrast, in 129T mice, histidine was decreased by both antibiotics. L-histamine, N-acetyl-histamine, histadinal, histadinol, 1-methyl-histamine, and anserine in the cecum were all decreased by an HFD and not rescued by either antibiotic. Of these, only L-histamine and anserine can be made in mammalian cells and were found in the plasma, and both tended to go up, not down. However, N-acetylhistamine showed identical patterns in the plasma and cecum, suggesting that the levels of this metabolite in the plasma are purely derived from gut microbial metabolism. |
|
Formal Description Interaction-ID: 89182 |
|
| Comment | In the cecum, histidine levels were not affected by an HFD, but in mice from Jax (B6J and 129J), histidine was increased by vancomycin and decreased by metronidazole treatment. By contrast, in 129T mice, histidine was decreased by both antibiotics. L-histamine, N-acetyl-histamine, histadinal, histadinol, 1-methyl-histamine, and anserine in the cecum were all decreased by an HFD and not rescued by either antibiotic. Of these, only L-histamine and anserine can be made in mammalian cells and were found in the plasma, and both tended to go up, not down. However, N-acetylhistamine showed identical patterns in the plasma and cecum, suggesting that the levels of this metabolite in the plasma are purely derived from gut microbial metabolism. |
|
Formal Description Interaction-ID: 89183 |
|
| Comment | Histidine can also be converted to urocanate and imidazole derivatives by both bacteria and, to some extent, mammalian cells. In the cecum, urocanate showed a dramatic decrease with both antibiotics, whereas dihydrourocanate (imidazole proprionate), a product of microbial but not murine metabolism, showed a variable decrease with an HFD but rose to above chow diet levels in HFD-fed mice on metronidazole, and this was mirrored almost exactly in the plasma. Urocanate can be converted to glutamic acid, isoglutamate, and alpha-ketoglutarate, but each of these showed unique patterns. Thus, the cecal and plasma levels of alpha-ketoglutarate were decreased by the HFD and further decreased in the cecum by both antibiotics, whereas the plasma levels of alpha-ketoglutarate were rescued by antibiotics. Isoglutamate in the cecum was selectively increased by metronidazole treatment in all strains of mice, indicating a role of gut microbes resistant to metronidazole in the production of this metabolite; however, isoglutamate was not detected in the blood. Thus, among histidine metabolites, only the blood levels of N-acetylhistamine and dihydrourocanate, and to some extent alpha-ketoglutarate, appear to be determined primarily by what is made or available in the gut. |
|
Formal Description Interaction-ID: 89184 |
|
| Comment | Histidine can also be converted to urocanate and imidazole derivatives by both bacteria and, to some extent, mammalian cells. In the cecum, urocanate showed a dramatic decrease with both antibiotics, whereas dihydrourocanate (imidazole proprionate), a product of microbial but not murine metabolism, showed a variable decrease with an HFD but rose to above chow diet levels in HFD-fed mice on metronidazole, and this was mirrored almost exactly in the plasma. Urocanate can be converted to glutamic acid, isoglutamate, and alpha-ketoglutarate, but each of these showed unique patterns. Thus, the cecal and plasma levels of alpha-ketoglutarate were decreased by the HFD and further decreased in the cecum by both antibiotics, whereas the plasma levels of alpha-ketoglutarate were rescued by antibiotics. Isoglutamate in the cecum was selectively increased by metronidazole treatment in all strains of mice, indicating a role of gut microbes resistant to metronidazole in the production of this metabolite; however, isoglutamate was not detected in the blood. Thus, among histidine metabolites, only the blood levels of N-acetylhistamine and dihydrourocanate, and to some extent alpha-ketoglutarate, appear to be determined primarily by what is made or available in the gut. |
|
Formal Description Interaction-ID: 89185 |
environment high-fat diet decreases_quantity of drug/chemical compound |
| Comment | Histidine can also be converted to urocanate and imidazole derivatives by both bacteria and, to some extent, mammalian cells. In the cecum, urocanate showed a dramatic decrease with both antibiotics, whereas dihydrourocanate (imidazole proprionate), a product of microbial but not murine metabolism, showed a variable decrease with an HFD but rose to above chow diet levels in HFD-fed mice on metronidazole, and this was mirrored almost exactly in the plasma. Urocanate can be converted to glutamic acid, isoglutamate, and alpha-ketoglutarate, but each of these showed unique patterns. Thus, the cecal and plasma levels of alpha-ketoglutarate were decreased by the HFD and further decreased in the cecum by both antibiotics, whereas the plasma levels of alpha-ketoglutarate were rescued by antibiotics. Isoglutamate in the cecum was selectively increased by metronidazole treatment in all strains of mice, indicating a role of gut microbes resistant to metronidazole in the production of this metabolite; however, isoglutamate was not detected in the blood. Thus, among histidine metabolites, only the blood levels of N-acetylhistamine and dihydrourocanate, and to some extent alpha-ketoglutarate, appear to be determined primarily by what is made or available in the gut. |
|
Formal Description Interaction-ID: 89186 |
environment metronidazole intake increases_quantity of drug/chemical compound |
| Comment | Histidine can also be converted to urocanate and imidazole derivatives by both bacteria and, to some extent, mammalian cells. In the cecum, urocanate showed a dramatic decrease with both antibiotics, whereas dihydrourocanate (imidazole proprionate), a product of microbial but not murine metabolism, showed a variable decrease with an HFD but rose to above chow diet levels in HFD-fed mice on metronidazole, and this was mirrored almost exactly in the plasma. Urocanate can be converted to glutamic acid, isoglutamate, and alpha-ketoglutarate, but each of these showed unique patterns. Thus, the cecal and plasma levels of alpha-ketoglutarate were decreased by the HFD and further decreased in the cecum by both antibiotics, whereas the plasma levels of alpha-ketoglutarate were rescued by antibiotics. Isoglutamate in the cecum was selectively increased by metronidazole treatment in all strains of mice, indicating a role of gut microbes resistant to metronidazole in the production of this metabolite; however, isoglutamate was not detected in the blood. Thus, among histidine metabolites, only the blood levels of N-acetylhistamine and dihydrourocanate, and to some extent alpha-ketoglutarate, appear to be determined primarily by what is made or available in the gut. |
|
Formal Description Interaction-ID: 89187 |
environment high-fat diet decreases_quantity of drug/chemical compound |
| Comment | Histidine can also be converted to urocanate and imidazole derivatives by both bacteria and, to some extent, mammalian cells. In the cecum, urocanate showed a dramatic decrease with both antibiotics, whereas dihydrourocanate (imidazole proprionate), a product of microbial but not murine metabolism, showed a variable decrease with an HFD but rose to above chow diet levels in HFD-fed mice on metronidazole, and this was mirrored almost exactly in the plasma. Urocanate can be converted to glutamic acid, isoglutamate, and alpha-ketoglutarate, but each of these showed unique patterns. Thus, the cecal and plasma levels of alpha-ketoglutarate were decreased by the HFD and further decreased in the cecum by both antibiotics, whereas the plasma levels of alpha-ketoglutarate were rescued by antibiotics. Isoglutamate in the cecum was selectively increased by metronidazole treatment in all strains of mice, indicating a role of gut microbes resistant to metronidazole in the production of this metabolite; however, isoglutamate was not detected in the blood. Thus, among histidine metabolites, only the blood levels of N-acetylhistamine and dihydrourocanate, and to some extent alpha-ketoglutarate, appear to be determined primarily by what is made or available in the gut. |
|
Formal Description Interaction-ID: 89188 |
|
| Comment | Histidine can also be converted to urocanate and imidazole derivatives by both bacteria and, to some extent, mammalian cells. In the cecum, urocanate showed a dramatic decrease with both antibiotics, whereas dihydrourocanate (imidazole proprionate), a product of microbial but not murine metabolism, showed a variable decrease with an HFD but rose to above chow diet levels in HFD-fed mice on metronidazole, and this was mirrored almost exactly in the plasma. Urocanate can be converted to glutamic acid, isoglutamate, and alpha-ketoglutarate, but each of these showed unique patterns. Thus, the cecal and plasma levels of alpha-ketoglutarate were decreased by the HFD and further decreased in the cecum by both antibiotics, whereas the plasma levels of alpha-ketoglutarate were rescued by antibiotics. Isoglutamate in the cecum was selectively increased by metronidazole treatment in all strains of mice, indicating a role of gut microbes resistant to metronidazole in the production of this metabolite; however, isoglutamate was not detected in the blood. Thus, among histidine metabolites, only the blood levels of N-acetylhistamine and dihydrourocanate, and to some extent alpha-ketoglutarate, appear to be determined primarily by what is made or available in the gut. |
|
Formal Description Interaction-ID: 89189 |
environment antibiotic intake increases_quantity of drug/chemical compound |
| Comment | Histidine can also be converted to urocanate and imidazole derivatives by both bacteria and, to some extent, mammalian cells. In the cecum, urocanate showed a dramatic decrease with both antibiotics, whereas dihydrourocanate (imidazole proprionate), a product of microbial but not murine metabolism, showed a variable decrease with an HFD but rose to above chow diet levels in HFD-fed mice on metronidazole, and this was mirrored almost exactly in the plasma. Urocanate can be converted to glutamic acid, isoglutamate, and alpha-ketoglutarate, but each of these showed unique patterns. Thus, the cecal and plasma levels of alpha-ketoglutarate were decreased by the HFD and further decreased in the cecum by both antibiotics, whereas the plasma levels of alpha-ketoglutarate were rescued by antibiotics. Isoglutamate in the cecum was selectively increased by metronidazole treatment in all strains of mice, indicating a role of gut microbes resistant to metronidazole in the production of this metabolite; however, isoglutamate was not detected in the blood. Thus, among histidine metabolites, only the blood levels of N-acetylhistamine and dihydrourocanate, and to some extent alpha-ketoglutarate, appear to be determined primarily by what is made or available in the gut. |
|
Formal Description Interaction-ID: 89191 |
|
| Comment | Aromatic amino acids have been linked to insulin resistance and showed multiple pathway-specific changes. Tryptophan levels in the cecum were decreased by metronidazole in all strains and by vancomycin in 129T mice, indicating the role of gut microbiota in tryptophan metabolism; however, this was not reflected by changes in the plasma. On the other hand, indole 3-acetate in the cecum decreased moderately with an HFD and markedly with both antibiotics, and this was mirrored in the plasma, indicating a strong dependence of this metabolite on the gut microbiota. 5-Hydroxytryptophan was increased in the cecum and plasma by an HFD, and anthranilate in the cecum and plasma were reduced in all vancomycin-treated groups. Likewise, although 3-indoleproprionic acid was not detected in the cecum, in the plasma, it was reduced to undetectable levels on an HFD or an HFD with antibiotics, suggesting that different tryptophan metabolites are regulated by the gut microbiota, but this affects the plasma levels for only some of these. |
|
Formal Description Interaction-ID: 89192 |
|
| Comment | Aromatic amino acids have been linked to insulin resistance and showed multiple pathway-specific changes. Tryptophan levels in the cecum were decreased by metronidazole in all strains and by vancomycin in 129T mice, indicating the role of gut microbiota in tryptophan metabolism; however, this was not reflected by changes in the plasma. On the other hand, indole 3-acetate in the cecum decreased moderately with an HFD and markedly with both antibiotics, and this was mirrored in the plasma, indicating a strong dependence of this metabolite on the gut microbiota. 5-Hydroxytryptophan was increased in the cecum and plasma by an HFD, and anthranilate in the cecum and plasma were reduced in all vancomycin-treated groups. Likewise, although 3-indoleproprionic acid was not detected in the cecum, in the plasma, it was reduced to undetectable levels on an HFD or an HFD with antibiotics, suggesting that different tryptophan metabolites are regulated by the gut microbiota, but this affects the plasma levels for only some of these. |
|
Formal Description Interaction-ID: 89195 |
environment vancomycin intake decreases_quantity of drug/chemical compound |
| Comment | Aromatic amino acids have been linked to insulin resistance and showed multiple pathway-specific changes. Tryptophan levels in the cecum were decreased by metronidazole in all strains and by vancomycin in 129T mice, indicating the role of gut microbiota in tryptophan metabolism; however, this was not reflected by changes in the plasma. On the other hand, indole 3-acetate in the cecum decreased moderately with an HFD and markedly with both antibiotics, and this was mirrored in the plasma, indicating a strong dependence of this metabolite on the gut microbiota. 5-Hydroxytryptophan was increased in the cecum and plasma by an HFD, and anthranilate in the cecum and plasma were reduced in all vancomycin-treated groups. Likewise, although 3-indoleproprionic acid was not detected in the cecum, in the plasma, it was reduced to undetectable levels on an HFD or an HFD with antibiotics, suggesting that different tryptophan metabolites are regulated by the gut microbiota, but this affects the plasma levels for only some of these. |
|
Formal Description Interaction-ID: 89196 |
environment high-fat diet decreases_quantity of drug/chemical compound |
| Comment | Aromatic amino acids have been linked to insulin resistance and showed multiple pathway-specific changes. Tryptophan levels in the cecum were decreased by metronidazole in all strains and by vancomycin in 129T mice, indicating the role of gut microbiota in tryptophan metabolism; however, this was not reflected by changes in the plasma. On the other hand, indole 3-acetate in the cecum decreased moderately with an HFD and markedly with both antibiotics, and this was mirrored in the plasma, indicating a strong dependence of this metabolite on the gut microbiota. 5-Hydroxytryptophan was increased in the cecum and plasma by an HFD, and anthranilate in the cecum and plasma were reduced in all vancomycin-treated groups. Likewise, although 3-indoleproprionic acid was not detected in the cecum, in the plasma, it was reduced to undetectable levels on an HFD or an HFD with antibiotics, suggesting that different tryptophan metabolites are regulated by the gut microbiota, but this affects the plasma levels for only some of these. |
|
Formal Description Interaction-ID: 89197 |
environment antibiotic intake decreases_quantity of drug/chemical compound |
| Comment | Aromatic amino acids have been linked to insulin resistance and showed multiple pathway-specific changes. Tryptophan levels in the cecum were decreased by metronidazole in all strains and by vancomycin in 129T mice, indicating the role of gut microbiota in tryptophan metabolism; however, this was not reflected by changes in the plasma. On the other hand, indole 3-acetate in the cecum decreased moderately with an HFD and markedly with both antibiotics, and this was mirrored in the plasma, indicating a strong dependence of this metabolite on the gut microbiota. 5-Hydroxytryptophan was increased in the cecum and plasma by an HFD, and anthranilate in the cecum and plasma were reduced in all vancomycin-treated groups. Likewise, although 3-indoleproprionic acid was not detected in the cecum, in the plasma, it was reduced to undetectable levels on an HFD or an HFD with antibiotics, suggesting that different tryptophan metabolites are regulated by the gut microbiota, but this affects the plasma levels for only some of these. |
|
Formal Description Interaction-ID: 89198 |
environment high-fat diet increases_quantity of drug/chemical compound |
| Comment | Aromatic amino acids have been linked to insulin resistance and showed multiple pathway-specific changes. Tryptophan levels in the cecum were decreased by metronidazole in all strains and by vancomycin in 129T mice, indicating the role of gut microbiota in tryptophan metabolism; however, this was not reflected by changes in the plasma. On the other hand, indole 3-acetate in the cecum decreased moderately with an HFD and markedly with both antibiotics, and this was mirrored in the plasma, indicating a strong dependence of this metabolite on the gut microbiota. 5-Hydroxytryptophan was increased in the cecum and plasma by an HFD, and anthranilate in the cecum and plasma were reduced in all vancomycin-treated groups. Likewise, although 3-indoleproprionic acid was not detected in the cecum, in the plasma, it was reduced to undetectable levels on an HFD or an HFD with antibiotics, suggesting that different tryptophan metabolites are regulated by the gut microbiota, but this affects the plasma levels for only some of these. |
|
Formal Description Interaction-ID: 89199 |
environment vancomycin intake decreases_quantity of drug/chemical compound |
| Comment | In the cecum, phenylalanine was unchanged by an HFD but decreased by both antibiotics, indicating a role for the gut microbiota, whereas in the plasma, phenylalanine was decreased by vancomycin in B6J mice and increased by metronidazole in all strains. On the other hand, phenylacetylglycine in the cecum was markedly decreased by both antibiotics in all strains, consistent with its role as a known gut microbial metabolite, with virtually identical changes in the plasma. Hippurate was markedly decreased in the cecum and plasma by an HFD in all strains but not rescued by antibiotics. Tyrosine levels in the cecum were decreased by vancomycin in B6J and 129T mice and by metronidazole in all three strains but increased in the plasma. Tyramine levels in the cecum were decreased by an HFD, further decreased by vancomycin, and increased to above chow levels by metronidazole, but these occurred with no consistent changes in the plasma. Thus, although the intestinal levels of phenylalanine, phenylacetylglycine, phenylacetylglutamine, tyrosine, and tyramine are dependent on the gut microbiota, gut metabolism is the primary driver of blood levels of phenylacetylglycine and, to some extent, hippurate. |
|
Formal Description Interaction-ID: 89200 |
|
| Comment | In the cecum, phenylalanine was unchanged by an HFD but decreased by both antibiotics, indicating a role for the gut microbiota, whereas in the plasma, phenylalanine was decreased by vancomycin in B6J mice and increased by metronidazole in all strains. On the other hand, phenylacetylglycine in the cecum was markedly decreased by both antibiotics in all strains, consistent with its role as a known gut microbial metabolite, with virtually identical changes in the plasma. Hippurate was markedly decreased in the cecum and plasma by an HFD in all strains but not rescued by antibiotics. Tyrosine levels in the cecum were decreased by vancomycin in B6J and 129T mice and by metronidazole in all three strains but increased in the plasma. Tyramine levels in the cecum were decreased by an HFD, further decreased by vancomycin, and increased to above chow levels by metronidazole, but these occurred with no consistent changes in the plasma. Thus, although the intestinal levels of phenylalanine, phenylacetylglycine, phenylacetylglutamine, tyrosine, and tyramine are dependent on the gut microbiota, gut metabolism is the primary driver of blood levels of phenylacetylglycine and, to some extent, hippurate. |
|
Formal Description Interaction-ID: 89203 |
environment vancomycin intake decreases_quantity of drug/chemical compound |
| Comment | In the cecum, phenylalanine was unchanged by an HFD but decreased by both antibiotics, indicating a role for the gut microbiota, whereas in the plasma, phenylalanine was decreased by vancomycin in B6J mice and increased by metronidazole in all strains. On the other hand, phenylacetylglycine in the cecum was markedly decreased by both antibiotics in all strains, consistent with its role as a known gut microbial metabolite, with virtually identical changes in the plasma. Hippurate was markedly decreased in the cecum and plasma by an HFD in all strains but not rescued by antibiotics. Tyrosine levels in the cecum were decreased by vancomycin in B6J and 129T mice and by metronidazole in all three strains but increased in the plasma. Tyramine levels in the cecum were decreased by an HFD, further decreased by vancomycin, and increased to above chow levels by metronidazole, but these occurred with no consistent changes in the plasma. Thus, although the intestinal levels of phenylalanine, phenylacetylglycine, phenylacetylglutamine, tyrosine, and tyramine are dependent on the gut microbiota, gut metabolism is the primary driver of blood levels of phenylacetylglycine and, to some extent, hippurate. |
|
Formal Description Interaction-ID: 89204 |
environment metronidazole intake increases_quantity of drug/chemical compound |
| Comment | In the cecum, phenylalanine was unchanged by an HFD but decreased by both antibiotics, indicating a role for the gut microbiota, whereas in the plasma, phenylalanine was decreased by vancomycin in B6J mice and increased by metronidazole in all strains. On the other hand, phenylacetylglycine in the cecum was markedly decreased by both antibiotics in all strains, consistent with its role as a known gut microbial metabolite, with virtually identical changes in the plasma. Hippurate was markedly decreased in the cecum and plasma by an HFD in all strains but not rescued by antibiotics. Tyrosine levels in the cecum were decreased by vancomycin in B6J and 129T mice and by metronidazole in all three strains but increased in the plasma. Tyramine levels in the cecum were decreased by an HFD, further decreased by vancomycin, and increased to above chow levels by metronidazole, but these occurred with no consistent changes in the plasma. Thus, although the intestinal levels of phenylalanine, phenylacetylglycine, phenylacetylglutamine, tyrosine, and tyramine are dependent on the gut microbiota, gut metabolism is the primary driver of blood levels of phenylacetylglycine and, to some extent, hippurate. |
|
Formal Description Interaction-ID: 89205 |
environment antibiotic intake decreases_quantity of drug/chemical compound |
| Comment | In the cecum, phenylalanine was unchanged by an HFD but decreased by both antibiotics, indicating a role for the gut microbiota, whereas in the plasma, phenylalanine was decreased by vancomycin in B6J mice and increased by metronidazole in all strains. On the other hand, phenylacetylglycine in the cecum was markedly decreased by both antibiotics in all strains, consistent with its role as a known gut microbial metabolite, with virtually identical changes in the plasma. Hippurate was markedly decreased in the cecum and plasma by an HFD in all strains but not rescued by antibiotics. Tyrosine levels in the cecum were decreased by vancomycin in B6J and 129T mice and by metronidazole in all three strains but increased in the plasma. Tyramine levels in the cecum were decreased by an HFD, further decreased by vancomycin, and increased to above chow levels by metronidazole, but these occurred with no consistent changes in the plasma. Thus, although the intestinal levels of phenylalanine, phenylacetylglycine, phenylacetylglutamine, tyrosine, and tyramine are dependent on the gut microbiota, gut metabolism is the primary driver of blood levels of phenylacetylglycine and, to some extent, hippurate. |
|
Formal Description Interaction-ID: 89211 |
environment high-fat diet decreases_quantity of drug/chemical compound |
| Comment | In the cecum, phenylalanine was unchanged by an HFD but decreased by both antibiotics, indicating a role for the gut microbiota, whereas in the plasma, phenylalanine was decreased by vancomycin in B6J mice and increased by metronidazole in all strains. On the other hand, phenylacetylglycine in the cecum was markedly decreased by both antibiotics in all strains, consistent with its role as a known gut microbial metabolite, with virtually identical changes in the plasma. Hippurate was markedly decreased in the cecum and plasma by an HFD in all strains but not rescued by antibiotics. Tyrosine levels in the cecum were decreased by vancomycin in B6J and 129T mice and by metronidazole in all three strains but increased in the plasma. Tyramine levels in the cecum were decreased by an HFD, further decreased by vancomycin, and increased to above chow levels by metronidazole, but these occurred with no consistent changes in the plasma. Thus, although the intestinal levels of phenylalanine, phenylacetylglycine, phenylacetylglutamine, tyrosine, and tyramine are dependent on the gut microbiota, gut metabolism is the primary driver of blood levels of phenylacetylglycine and, to some extent, hippurate. |
|
Formal Description Interaction-ID: 89212 |
environment vancomycin intake decreases_quantity of drug/chemical compound |
| Comment | In the cecum, phenylalanine was unchanged by an HFD but decreased by both antibiotics, indicating a role for the gut microbiota, whereas in the plasma, phenylalanine was decreased by vancomycin in B6J mice and increased by metronidazole in all strains. On the other hand, phenylacetylglycine in the cecum was markedly decreased by both antibiotics in all strains, consistent with its role as a known gut microbial metabolite, with virtually identical changes in the plasma. Hippurate was markedly decreased in the cecum and plasma by an HFD in all strains but not rescued by antibiotics. Tyrosine levels in the cecum were decreased by vancomycin in B6J and 129T mice and by metronidazole in all three strains but increased in the plasma. Tyramine levels in the cecum were decreased by an HFD, further decreased by vancomycin, and increased to above chow levels by metronidazole, but these occurred with no consistent changes in the plasma. Thus, although the intestinal levels of phenylalanine, phenylacetylglycine, phenylacetylglutamine, tyrosine, and tyramine are dependent on the gut microbiota, gut metabolism is the primary driver of blood levels of phenylacetylglycine and, to some extent, hippurate. |
|
Formal Description Interaction-ID: 89213 |
|
| Comment | In the cecum, phenylalanine was unchanged by an HFD but decreased by both antibiotics, indicating a role for the gut microbiota, whereas in the plasma, phenylalanine was decreased by vancomycin in B6J mice and increased by metronidazole in all strains. On the other hand, phenylacetylglycine in the cecum was markedly decreased by both antibiotics in all strains, consistent with its role as a known gut microbial metabolite, with virtually identical changes in the plasma. Hippurate was markedly decreased in the cecum and plasma by an HFD in all strains but not rescued by antibiotics. Tyrosine levels in the cecum were decreased by vancomycin in B6J and 129T mice and by metronidazole in all three strains but increased in the plasma. Tyramine levels in the cecum were decreased by an HFD, further decreased by vancomycin, and increased to above chow levels by metronidazole, but these occurred with no consistent changes in the plasma. Thus, although the intestinal levels of phenylalanine, phenylacetylglycine, phenylacetylglutamine, tyrosine, and tyramine are dependent on the gut microbiota, gut metabolism is the primary driver of blood levels of phenylacetylglycine and, to some extent, hippurate. |
|
Formal Description Interaction-ID: 89214 |
environment metronidazole intake increases_quantity of drug/chemical compound |
| Comment | In the cecum, phenylalanine was unchanged by an HFD but decreased by both antibiotics, indicating a role for the gut microbiota, whereas in the plasma, phenylalanine was decreased by vancomycin in B6J mice and increased by metronidazole in all strains. On the other hand, phenylacetylglycine in the cecum was markedly decreased by both antibiotics in all strains, consistent with its role as a known gut microbial metabolite, with virtually identical changes in the plasma. Hippurate was markedly decreased in the cecum and plasma by an HFD in all strains but not rescued by antibiotics. Tyrosine levels in the cecum were decreased by vancomycin in B6J and 129T mice and by metronidazole in all three strains but increased in the plasma. Tyramine levels in the cecum were decreased by an HFD, further decreased by vancomycin, and increased to above chow levels by metronidazole, but these occurred with no consistent changes in the plasma. Thus, although the intestinal levels of phenylalanine, phenylacetylglycine, phenylacetylglutamine, tyrosine, and tyramine are dependent on the gut microbiota, gut metabolism is the primary driver of blood levels of phenylacetylglycine and, to some extent, hippurate. |
|
Formal Description Interaction-ID: 89215 |
|
| Comment | In the cecum, phenylalanine was unchanged by an HFD but decreased by both antibiotics, indicating a role for the gut microbiota, whereas in the plasma, phenylalanine was decreased by vancomycin in B6J mice and increased by metronidazole in all strains. On the other hand, phenylacetylglycine in the cecum was markedly decreased by both antibiotics in all strains, consistent with its role as a known gut microbial metabolite, with virtually identical changes in the plasma. Hippurate was markedly decreased in the cecum and plasma by an HFD in all strains but not rescued by antibiotics. Tyrosine levels in the cecum were decreased by vancomycin in B6J and 129T mice and by metronidazole in all three strains but increased in the plasma. Tyramine levels in the cecum were decreased by an HFD, further decreased by vancomycin, and increased to above chow levels by metronidazole, but these occurred with no consistent changes in the plasma. Thus, although the intestinal levels of phenylalanine, phenylacetylglycine, phenylacetylglutamine, tyrosine, and tyramine are dependent on the gut microbiota, gut metabolism is the primary driver of blood levels of phenylacetylglycine and, to some extent, hippurate. |
|
Formal Description Interaction-ID: 89216 |
|
| Comment | In the cecum, phenylalanine was unchanged by an HFD but decreased by both antibiotics, indicating a role for the gut microbiota, whereas in the plasma, phenylalanine was decreased by vancomycin in B6J mice and increased by metronidazole in all strains. On the other hand, phenylacetylglycine in the cecum was markedly decreased by both antibiotics in all strains, consistent with its role as a known gut microbial metabolite, with virtually identical changes in the plasma. Hippurate was markedly decreased in the cecum and plasma by an HFD in all strains but not rescued by antibiotics. Tyrosine levels in the cecum were decreased by vancomycin in B6J and 129T mice and by metronidazole in all three strains but increased in the plasma. Tyramine levels in the cecum were decreased by an HFD, further decreased by vancomycin, and increased to above chow levels by metronidazole, but these occurred with no consistent changes in the plasma. Thus, although the intestinal levels of phenylalanine, phenylacetylglycine, phenylacetylglutamine, tyrosine, and tyramine are dependent on the gut microbiota, gut metabolism is the primary driver of blood levels of phenylacetylglycine and, to some extent, hippurate. |
|
Formal Description Interaction-ID: 89217 |
|
| Comment | The plasma levels of a number of metabolites showed strong positive correlations with insulin resistance, including aminoadipate, alpha-hydroxybutyrate, acetylglycine, C16-carnitine, N-carbamoyl-beta-alanine, thymidine, carnosine, 4-pyridoxate, C34:4 PC, and C30:0 PC. On the other hand, adipate, C34:2 PC plasmalogen, C36:2 PC plasmalogen, C38:6 PC plasmalogen, C58:6 triacylglycerol (TAG), C58:7 TAG, taurolithocholic acid, and guanidinoacetate all showed negative correlations with insulin resistance. Importantly, 2-aminoadipoate, alpha-hydroxybutyrate, and N-acetylglycine have also been previously identified in humans as potential biomarkers for diabetes risk and insulin resistance, as have patterns of lipids with lower fatty acyl carbon number and double bond content. |
|
Formal Description Interaction-ID: 89218 |
disease Insulin resistance increases_quantity of drug/chemical compound Aminoadipate |
| Comment | The plasma levels of a number of metabolites showed strong positive correlations with insulin resistance, including aminoadipate, alpha-hydroxybutyrate, acetylglycine, C16-carnitine, N-carbamoyl-beta-alanine, thymidine, carnosine, 4-pyridoxate, C34:4 PC, and C30:0 PC. On the other hand, adipate, C34:2 PC plasmalogen, C36:2 PC plasmalogen, C38:6 PC plasmalogen, C58:6 triacylglycerol (TAG), C58:7 TAG, taurolithocholic acid, and guanidinoacetate all showed negative correlations with insulin resistance. Importantly, 2-aminoadipoate, alpha-hydroxybutyrate, and N-acetylglycine have also been previously identified in humans as potential biomarkers for diabetes risk and insulin resistance, as have patterns of lipids with lower fatty acyl carbon number and double bond content. |
|
Formal Description Interaction-ID: 89219 |
disease Insulin resistance increases_quantity of drug/chemical compound |
| Comment | The plasma levels of a number of metabolites showed strong positive correlations with insulin resistance, including aminoadipate, alpha-hydroxybutyrate, acetylglycine, C16-carnitine, N-carbamoyl-beta-alanine, thymidine, carnosine, 4-pyridoxate, C34:4 PC, and C30:0 PC. On the other hand, adipate, C34:2 PC plasmalogen, C36:2 PC plasmalogen, C38:6 PC plasmalogen, C58:6 triacylglycerol (TAG), C58:7 TAG, taurolithocholic acid, and guanidinoacetate all showed negative correlations with insulin resistance. Importantly, 2-aminoadipoate, alpha-hydroxybutyrate, and N-acetylglycine have also been previously identified in humans as potential biomarkers for diabetes risk and insulin resistance, as have patterns of lipids with lower fatty acyl carbon number and double bond content. |
|
Formal Description Interaction-ID: 89220 |
disease Insulin resistance increases_quantity of drug/chemical compound Acetylglycine |
| Comment | The plasma levels of a number of metabolites showed strong positive correlations with insulin resistance, including aminoadipate, alpha-hydroxybutyrate, acetylglycine, C16-carnitine, N-carbamoyl-beta-alanine, thymidine, carnosine, 4-pyridoxate, C34:4 PC, and C30:0 PC. On the other hand, adipate, C34:2 PC plasmalogen, C36:2 PC plasmalogen, C38:6 PC plasmalogen, C58:6 triacylglycerol (TAG), C58:7 TAG, taurolithocholic acid, and guanidinoacetate all showed negative correlations with insulin resistance. Importantly, 2-aminoadipoate, alpha-hydroxybutyrate, and N-acetylglycine have also been previously identified in humans as potential biomarkers for diabetes risk and insulin resistance, as have patterns of lipids with lower fatty acyl carbon number and double bond content. |
|
Formal Description Interaction-ID: 89221 |
disease Insulin resistance increases_quantity of drug/chemical compound |
| Comment | The plasma levels of a number of metabolites showed strong positive correlations with insulin resistance, including aminoadipate, alpha-hydroxybutyrate, acetylglycine, C16-carnitine, N-carbamoyl-beta-alanine, thymidine, carnosine, 4-pyridoxate, C34:4 PC, and C30:0 PC. On the other hand, adipate, C34:2 PC plasmalogen, C36:2 PC plasmalogen, C38:6 PC plasmalogen, C58:6 triacylglycerol (TAG), C58:7 TAG, taurolithocholic acid, and guanidinoacetate all showed negative correlations with insulin resistance. Importantly, 2-aminoadipoate, alpha-hydroxybutyrate, and N-acetylglycine have also been previously identified in humans as potential biomarkers for diabetes risk and insulin resistance, as have patterns of lipids with lower fatty acyl carbon number and double bond content. |
|
Formal Description Interaction-ID: 89222 |
disease Insulin resistance increases_quantity of drug/chemical compound |
| Comment | The plasma levels of a number of metabolites showed strong positive correlations with insulin resistance, including aminoadipate, alpha-hydroxybutyrate, acetylglycine, C16-carnitine, N-carbamoyl-beta-alanine, thymidine, carnosine, 4-pyridoxate, C34:4 PC, and C30:0 PC. On the other hand, adipate, C34:2 PC plasmalogen, C36:2 PC plasmalogen, C38:6 PC plasmalogen, C58:6 triacylglycerol (TAG), C58:7 TAG, taurolithocholic acid, and guanidinoacetate all showed negative correlations with insulin resistance. Importantly, 2-aminoadipoate, alpha-hydroxybutyrate, and N-acetylglycine have also been previously identified in humans as potential biomarkers for diabetes risk and insulin resistance, as have patterns of lipids with lower fatty acyl carbon number and double bond content. |
|
Formal Description Interaction-ID: 89223 |
|
| Comment | The plasma levels of a number of metabolites showed strong positive correlations with insulin resistance, including aminoadipate, alpha-hydroxybutyrate, acetylglycine, C16-carnitine, N-carbamoyl-beta-alanine, thymidine, carnosine, 4-pyridoxate, C34:4 PC, and C30:0 PC. On the other hand, adipate, C34:2 PC plasmalogen, C36:2 PC plasmalogen, C38:6 PC plasmalogen, C58:6 triacylglycerol (TAG), C58:7 TAG, taurolithocholic acid, and guanidinoacetate all showed negative correlations with insulin resistance. Importantly, 2-aminoadipoate, alpha-hydroxybutyrate, and N-acetylglycine have also been previously identified in humans as potential biomarkers for diabetes risk and insulin resistance, as have patterns of lipids with lower fatty acyl carbon number and double bond content. |
|
Formal Description Interaction-ID: 89224 |
|
| Comment | The plasma levels of a number of metabolites showed strong positive correlations with insulin resistance, including aminoadipate, alpha-hydroxybutyrate, acetylglycine, C16-carnitine, N-carbamoyl-beta-alanine, thymidine, carnosine, 4-pyridoxate, C34:4 PC, and C30:0 PC. On the other hand, adipate, C34:2 PC plasmalogen, C36:2 PC plasmalogen, C38:6 PC plasmalogen, C58:6 triacylglycerol (TAG), C58:7 TAG, taurolithocholic acid, and guanidinoacetate all showed negative correlations with insulin resistance. Importantly, 2-aminoadipoate, alpha-hydroxybutyrate, and N-acetylglycine have also been previously identified in humans as potential biomarkers for diabetes risk and insulin resistance, as have patterns of lipids with lower fatty acyl carbon number and double bond content. |
|
Formal Description Interaction-ID: 89225 |
disease Insulin resistance increases_quantity of drug/chemical compound |
| Comment | The plasma levels of a number of metabolites showed strong positive correlations with insulin resistance, including aminoadipate, alpha-hydroxybutyrate, acetylglycine, C16-carnitine, N-carbamoyl-beta-alanine, thymidine, carnosine, 4-pyridoxate, C34:4 PC, and C30:0 PC. On the other hand, adipate, C34:2 PC plasmalogen, C36:2 PC plasmalogen, C38:6 PC plasmalogen, C58:6 triacylglycerol (TAG), C58:7 TAG, taurolithocholic acid, and guanidinoacetate all showed negative correlations with insulin resistance. Importantly, 2-aminoadipoate, alpha-hydroxybutyrate, and N-acetylglycine have also been previously identified in humans as potential biomarkers for diabetes risk and insulin resistance, as have patterns of lipids with lower fatty acyl carbon number and double bond content. |
|
Formal Description Interaction-ID: 89226 |
disease Insulin resistance increases_quantity of drug/chemical compound PC C34:4 |
| Comment | The plasma levels of a number of metabolites showed strong positive correlations with insulin resistance, including aminoadipate, alpha-hydroxybutyrate, acetylglycine, C16-carnitine, N-carbamoyl-beta-alanine, thymidine, carnosine, 4-pyridoxate, C34:4 PC, and C30:0 PC. On the other hand, adipate, C34:2 PC plasmalogen, C36:2 PC plasmalogen, C38:6 PC plasmalogen, C58:6 triacylglycerol (TAG), C58:7 TAG, taurolithocholic acid, and guanidinoacetate all showed negative correlations with insulin resistance. Importantly, 2-aminoadipoate, alpha-hydroxybutyrate, and N-acetylglycine have also been previously identified in humans as potential biomarkers for diabetes risk and insulin resistance, as have patterns of lipids with lower fatty acyl carbon number and double bond content. |
|
Formal Description Interaction-ID: 89227 |
disease Insulin resistance increases_quantity of drug/chemical compound PC C30:0 |
| Comment | The plasma levels of a number of metabolites showed strong positive correlations with insulin resistance, including aminoadipate, alpha-hydroxybutyrate, acetylglycine, C16-carnitine, N-carbamoyl-beta-alanine, thymidine, carnosine, 4-pyridoxate, C34:4 PC, and C30:0 PC. On the other hand, adipate, C34:2 PC plasmalogen, C36:2 PC plasmalogen, C38:6 PC plasmalogen, C58:6 triacylglycerol (TAG), C58:7 TAG, taurolithocholic acid, and guanidinoacetate all showed negative correlations with insulin resistance. Importantly, 2-aminoadipoate, alpha-hydroxybutyrate, and N-acetylglycine have also been previously identified in humans as potential biomarkers for diabetes risk and insulin resistance, as have patterns of lipids with lower fatty acyl carbon number and double bond content. |
|
Formal Description Interaction-ID: 89228 |
|
| Comment | The plasma levels of a number of metabolites showed strong positive correlations with insulin resistance, including aminoadipate, alpha-hydroxybutyrate, acetylglycine, C16-carnitine, N-carbamoyl-beta-alanine, thymidine, carnosine, 4-pyridoxate, C34:4 PC, and C30:0 PC. On the other hand, adipate, C34:2 PC plasmalogen, C36:2 PC plasmalogen, C38:6 PC plasmalogen, C58:6 triacylglycerol (TAG), C58:7 TAG, taurolithocholic acid, and guanidinoacetate all showed negative correlations with insulin resistance. Importantly, 2-aminoadipoate, alpha-hydroxybutyrate, and N-acetylglycine have also been previously identified in humans as potential biomarkers for diabetes risk and insulin resistance, as have patterns of lipids with lower fatty acyl carbon number and double bond content. |
|
Formal Description Interaction-ID: 89229 |
disease Insulin resistance decreases_quantity of drug/chemical compound PC C34:2 plasmalogen |
| Comment | The plasma levels of a number of metabolites showed strong positive correlations with insulin resistance, including aminoadipate, alpha-hydroxybutyrate, acetylglycine, C16-carnitine, N-carbamoyl-beta-alanine, thymidine, carnosine, 4-pyridoxate, C34:4 PC, and C30:0 PC. On the other hand, adipate, C34:2 PC plasmalogen, C36:2 PC plasmalogen, C38:6 PC plasmalogen, C58:6 triacylglycerol (TAG), C58:7 TAG, taurolithocholic acid, and guanidinoacetate all showed negative correlations with insulin resistance. Importantly, 2-aminoadipoate, alpha-hydroxybutyrate, and N-acetylglycine have also been previously identified in humans as potential biomarkers for diabetes risk and insulin resistance, as have patterns of lipids with lower fatty acyl carbon number and double bond content. |
|
Formal Description Interaction-ID: 89230 |
disease Insulin resistance decreases_quantity of drug/chemical compound PC C36:2 plasmalogen |
| Comment | The plasma levels of a number of metabolites showed strong positive correlations with insulin resistance, including aminoadipate, alpha-hydroxybutyrate, acetylglycine, C16-carnitine, N-carbamoyl-beta-alanine, thymidine, carnosine, 4-pyridoxate, C34:4 PC, and C30:0 PC. On the other hand, adipate, C34:2 PC plasmalogen, C36:2 PC plasmalogen, C38:6 PC plasmalogen, C58:6 triacylglycerol (TAG), C58:7 TAG, taurolithocholic acid, and guanidinoacetate all showed negative correlations with insulin resistance. Importantly, 2-aminoadipoate, alpha-hydroxybutyrate, and N-acetylglycine have also been previously identified in humans as potential biomarkers for diabetes risk and insulin resistance, as have patterns of lipids with lower fatty acyl carbon number and double bond content. |
|
Formal Description Interaction-ID: 89231 |
disease Insulin resistance decreases_quantity of drug/chemical compound PC C38:6 plasmalogen |
| Comment | The plasma levels of a number of metabolites showed strong positive correlations with insulin resistance, including aminoadipate, alpha-hydroxybutyrate, acetylglycine, C16-carnitine, N-carbamoyl-beta-alanine, thymidine, carnosine, 4-pyridoxate, C34:4 PC, and C30:0 PC. On the other hand, adipate, C34:2 PC plasmalogen, C36:2 PC plasmalogen, C38:6 PC plasmalogen, C58:6 triacylglycerol (TAG), C58:7 TAG, taurolithocholic acid, and guanidinoacetate all showed negative correlations with insulin resistance. Importantly, 2-aminoadipoate, alpha-hydroxybutyrate, and N-acetylglycine have also been previously identified in humans as potential biomarkers for diabetes risk and insulin resistance, as have patterns of lipids with lower fatty acyl carbon number and double bond content. |
|
Formal Description Interaction-ID: 89232 |
disease Insulin resistance decreases_quantity of drug/chemical compound TAG(58:6) |
| Comment | The plasma levels of a number of metabolites showed strong positive correlations with insulin resistance, including aminoadipate, alpha-hydroxybutyrate, acetylglycine, C16-carnitine, N-carbamoyl-beta-alanine, thymidine, carnosine, 4-pyridoxate, C34:4 PC, and C30:0 PC. On the other hand, adipate, C34:2 PC plasmalogen, C36:2 PC plasmalogen, C38:6 PC plasmalogen, C58:6 triacylglycerol (TAG), C58:7 TAG, taurolithocholic acid, and guanidinoacetate all showed negative correlations with insulin resistance. Importantly, 2-aminoadipoate, alpha-hydroxybutyrate, and N-acetylglycine have also been previously identified in humans as potential biomarkers for diabetes risk and insulin resistance, as have patterns of lipids with lower fatty acyl carbon number and double bond content. |
|
Formal Description Interaction-ID: 89233 |
disease Insulin resistance decreases_quantity of drug/chemical compound TAG(58:7) |
| Comment | The plasma levels of a number of metabolites showed strong positive correlations with insulin resistance, including aminoadipate, alpha-hydroxybutyrate, acetylglycine, C16-carnitine, N-carbamoyl-beta-alanine, thymidine, carnosine, 4-pyridoxate, C34:4 PC, and C30:0 PC. On the other hand, adipate, C34:2 PC plasmalogen, C36:2 PC plasmalogen, C38:6 PC plasmalogen, C58:6 triacylglycerol (TAG), C58:7 TAG, taurolithocholic acid, and guanidinoacetate all showed negative correlations with insulin resistance. Importantly, 2-aminoadipoate, alpha-hydroxybutyrate, and N-acetylglycine have also been previously identified in humans as potential biomarkers for diabetes risk and insulin resistance, as have patterns of lipids with lower fatty acyl carbon number and double bond content. |
|
Formal Description Interaction-ID: 89234 |
disease Insulin resistance decreases_quantity of drug/chemical compound |
| Comment | The plasma levels of a number of metabolites showed strong positive correlations with insulin resistance, including aminoadipate, alpha-hydroxybutyrate, acetylglycine, C16-carnitine, N-carbamoyl-beta-alanine, thymidine, carnosine, 4-pyridoxate, C34:4 PC, and C30:0 PC. On the other hand, adipate, C34:2 PC plasmalogen, C36:2 PC plasmalogen, C38:6 PC plasmalogen, C58:6 triacylglycerol (TAG), C58:7 TAG, taurolithocholic acid, and guanidinoacetate all showed negative correlations with insulin resistance. Importantly, 2-aminoadipoate, alpha-hydroxybutyrate, and N-acetylglycine have also been previously identified in humans as potential biomarkers for diabetes risk and insulin resistance, as have patterns of lipids with lower fatty acyl carbon number and double bond content. |
|
Formal Description Interaction-ID: 89235 |
disease Insulin resistance decreases_quantity of drug/chemical compound |