CIDeRplusGeneral Information:
| Id: | 6,151 |
| Diseases: |
Diabetes mellitus, type II
- [OMIM]
Insulin resistance |
| Mus musculus | |
| article | |
| Reference: | Raddatz K et al.(2012) Deletion of protein kinase Cepsilon in mice has limited effects on liver metabolite levels but alters fasting ketogenesis and gluconeogenesis Diabetologia 55: 2789-2793 [PMID: 22814763] |
Interaction Information:
| Comment | Protein kinase C epsilon (PKCepsilon) is emerging as a key mediator of lipid-induced insulin resistance in liver and hepatic lipid metabolism itself. The levels of 20 compounds were altered similarly in livers from both WT and Prkce-/- high-fat-fed mice, indicating a consistent response to the high-fat diet. Alanine, ethanolamine and gamma-aminobutyric acid levels were reduced by approximately 50% by fat feeding, while tocopherol, sucrose and taurine levels were significantly increased. Prkce deletion resulted only in a reduction of 4-hydroxyproline and aspartate and an increase in glutamate. |
|
Formal Description Interaction-ID: 57532 |
|
| Comment | Protein kinase C epsilon (PKCepsilon) is emerging as a key mediator of lipid-induced insulin resistance in liver and hepatic lipid metabolism itself. The levels of 20 compounds were altered similarly in livers from both WT and Prkce-/- high-fat-fed mice, indicating a consistent response to the high-fat diet. Alanine, ethanolamine and gamma-aminobutyric acid levels were reduced by approximately 50% by fat feeding, while tocopherol, sucrose and taurine levels were significantly increased. Prkce deletion resulted only in a reduction of 4-hydroxyproline and aspartate and an increase in glutamate. |
|
Formal Description Interaction-ID: 57552 |
|
| Comment | Protein kinase C epsilon (PKCepsilon) is emerging as a key mediator of lipid-induced insulin resistance in liver and hepatic lipid metabolism itself. The levels of 20 compounds were altered similarly in livers from both WT and Prkce-/- high-fat-fed mice, indicating a consistent response to the high-fat diet. Alanine, ethanolamine and gamma-aminobutyric acid levels were reduced by approximately 50% by fat feeding, while tocopherol, sucrose and taurine levels were significantly increased. Prkce deletion resulted only in a reduction of 4-hydroxyproline and aspartate and an increase in glutamate. |
|
Formal Description Interaction-ID: 57553 |
|
| Drugbank entries | Show/Hide entries for |
| Comment | Protein kinase C epsilon (PKCepsilon) is emerging as a key mediator of lipid-induced insulin resistance in liver and hepatic lipid metabolism itself. The levels of 20 compounds were altered similarly in livers from both WT and Prkce-/- high-fat-fed mice, indicating a consistent response to the high-fat diet. Alanine, ethanolamine and gamma-aminobutyric acid levels were reduced by approximately 50% by fat feeding, while tocopherol, sucrose and taurine levels were significantly increased. Prkce deletion resulted only in a reduction of 4-hydroxyproline and aspartate and an increase in glutamate. |
|
Formal Description Interaction-ID: 57554 |
|
| Drugbank entries | Show/Hide entries for |
| Comment | Protein kinase C epsilon (PKCepsilon) is emerging as a key mediator of lipid-induced insulin resistance in liver and hepatic lipid metabolism itself. The levels of 20 compounds were altered similarly in livers from both WT and Prkce-/- high-fat-fed mice, indicating a consistent response to the high-fat diet. Alanine, ethanolamine and gamma-aminobutyric acid levels were reduced by approximately 50% by fat feeding, while tocopherol, sucrose and taurine levels were significantly increased. Prkce deletion resulted only in a reduction of 4-hydroxyproline and aspartate and an increase in glutamate. |
|
Formal Description Interaction-ID: 57555 |
|
| Comment | Protein kinase C epsilon (PKCepsilon) is emerging as a key mediator of lipid-induced insulin resistance in liver and hepatic lipid metabolism itself. The levels of 20 compounds were altered similarly in livers from both WT and Prkce-/- high-fat-fed mice, indicating a consistent response to the high-fat diet. Alanine, ethanolamine and gamma-aminobutyric acid levels were reduced by approximately 50% by fat feeding, while tocopherol, sucrose and taurine levels were significantly increased. Prkce deletion resulted only in a reduction of 4-hydroxyproline and aspartate and an increase in glutamate. |
|
Formal Description Interaction-ID: 57556 |
|
| Comment | Protein kinase C epsilon (PKCepsilon) is emerging as a key mediator of lipid-induced insulin resistance in liver and hepatic lipid metabolism itself. The levels of 20 compounds were altered similarly in livers from both WT and Prkce-/- high-fat-fed mice, indicating a consistent response to the high-fat diet. Alanine, ethanolamine and gamma-aminobutyric acid levels were reduced by approximately 50% by fat feeding, while tocopherol, sucrose and taurine levels were significantly increased. Prkce deletion resulted only in a reduction of 4-hydroxyproline and aspartate and an increase in glutamate. |
|
Formal Description Interaction-ID: 57557 |
|
| Comment | Protein kinase C epsilon (PKCepsilon) is emerging as a key mediator of lipid-induced insulin resistance in liver and hepatic lipid metabolism itself. The levels of 20 compounds were altered similarly in livers from both WT and Prkce-/- high-fat-fed mice, indicating a consistent response to the high-fat diet. Alanine, ethanolamine and gamma-aminobutyric acid levels were reduced by approximately 50% by fat feeding, while tocopherol, sucrose and taurine levels were significantly increased. Prkce deletion resulted only in a reduction of 4-hydroxyproline and aspartate and an increase in glutamate. |
|
Formal Description Interaction-ID: 57558 |
environment high-fat diet increases_quantity of drug/chemical compound |
| Comment | Protein kinase C epsilon (PKCepsilon) is emerging as a key mediator of lipid-induced insulin resistance in liver and hepatic lipid metabolism itself. The levels of 20 compounds were altered similarly in livers from both WT and Prkce-/- high-fat-fed mice, indicating a consistent response to the high-fat diet. Alanine, ethanolamine and gamma-aminobutyric acid levels were reduced by approximately 50% by fat feeding, while tocopherol, sucrose and taurine levels were significantly increased. Prkce deletion resulted only in a reduction of 4-hydroxyproline and aspartate and an increase in glutamate. |
|
Formal Description Interaction-ID: 57559 |
|
| Comment | Protein kinase C epsilon (PKCepsilon) is emerging as a key mediator of lipid-induced insulin resistance in liver and hepatic lipid metabolism itself. The levels of 20 compounds were altered similarly in livers from both WT and Prkce-/- high-fat-fed mice, indicating a consistent response to the high-fat diet. Alanine, ethanolamine and gamma-aminobutyric acid levels were reduced by approximately 50% by fat feeding, while tocopherol, sucrose and taurine levels were significantly increased. Prkce deletion resulted only in a reduction of 4-hydroxyproline and aspartate and an increase in glutamate. |
|
Formal Description Interaction-ID: 57560 |
environment high-fat diet increases_quantity of drug/chemical compound Tocopherol |
| Comment | Protein kinase C epsilon (PKCepsilon) is emerging as a key mediator of lipid-induced insulin resistance in liver and hepatic lipid metabolism itself. The levels of 20 compounds were altered similarly in livers from both WT and Prkce-/- high-fat-fed mice, indicating a consistent response to the high-fat diet. Alanine, ethanolamine and gamma-aminobutyric acid levels were reduced by approximately 50% by fat feeding, while tocopherol, sucrose and taurine levels were significantly increased. Prkce deletion resulted only in a reduction of 4-hydroxyproline and aspartate and an increase in glutamate. |
|
Formal Description Interaction-ID: 57561 |
|
| Drugbank entries | Show/Hide entries for |
| Comment | Protein kinase C epsilon (PKCepsilon) is emerging as a key mediator of lipid-induced insulin resistance in liver and hepatic lipid metabolism itself. The levels of 20 compounds were altered similarly in livers from both WT and Prkce-/- high-fat-fed mice, indicating a consistent response to the high-fat diet. Alanine, ethanolamine and gamma-aminobutyric acid levels were reduced by approximately 50% by fat feeding, while tocopherol, sucrose and taurine levels were significantly increased. Prkce deletion resulted only in a reduction of 4-hydroxyproline and aspartate and an increase in glutamate. |
|
Formal Description Interaction-ID: 57564 |
|
| Comment | Protein kinase C epsilon (PKCepsilon) is emerging as a key mediator of lipid-induced insulin resistance in liver and hepatic lipid metabolism itself. The levels of 20 compounds were altered similarly in livers from both WT and Prkce-/- high-fat-fed mice, indicating a consistent response to the high-fat diet. Alanine, ethanolamine and gamma-aminobutyric acid levels were reduced by approximately 50% by fat feeding, while tocopherol, sucrose and taurine levels were significantly increased. Prkce deletion resulted only in a reduction of 4-hydroxyproline and aspartate and an increase in glutamate. |
|
Formal Description Interaction-ID: 57565 |
|
| Comment | Protein kinase C epsilon (PKCepsilon) is emerging as a key mediator of lipid-induced insulin resistance in liver and hepatic lipid metabolism itself. The levels of 20 compounds were altered similarly in livers from both WT and Prkce-/- high-fat-fed mice, indicating a consistent response to the high-fat diet. Alanine, ethanolamine and gamma-aminobutyric acid levels were reduced by approximately 50% by fat feeding, while tocopherol, sucrose and taurine levels were significantly increased. Prkce deletion resulted only in a reduction of 4-hydroxyproline and aspartate and an increase in glutamate. |
|
Formal Description Interaction-ID: 57566 |
|
| Comment | Protein kinase C epsilon (PKCepsilon) is emerging as a key mediator of lipid-induced insulin resistance in liver and hepatic lipid metabolism itself. The levels of 20 compounds were altered similarly in livers from both WT and Prkce-/- high-fat-fed mice, indicating a consistent response to the high-fat diet. Alanine, ethanolamine and gamma-aminobutyric acid levels were reduced by approximately 50% by fat feeding, while tocopherol, sucrose and taurine levels were significantly increased. Prkce deletion resulted only in a reduction of 4-hydroxyproline and aspartate and an increase in glutamate. |
|
Formal Description Interaction-ID: 57567 |
|
| Comment | Protein kinase C epsilon (PKCepsilon) is emerging as a key mediator of lipid-induced insulin resistance in liver and hepatic lipid metabolism itself. The levels of 20 compounds were altered similarly in livers from both WT and Prkce-/- high-fat-fed mice, indicating a consistent response to the high-fat diet. Alanine, ethanolamine and gamma-aminobutyric acid levels were reduced by approximately 50% by fat feeding, while tocopherol, sucrose and taurine levels were significantly increased. Prkce deletion resulted only in a reduction of 4-hydroxyproline and aspartate and an increase in glutamate. |
|
Formal Description Interaction-ID: 57568 |
|
| Comment | Upon fasting, Prkce -/- mice were better able to maintain blood glucose levels and also exhibited lower levels of the ketone beta-hydroxybutyrate compared with WT mice. Upon fasting, Prkce deletion also resulted in lower liver and plasma lipids and a smaller reduction in fat pad mass. |
|
Formal Description Interaction-ID: 57570 |
|
| Comment | Upon fasting, Prkce -/- mice were better able to maintain blood glucose levels and also exhibited lower levels of the ketone beta-hydroxybutyrate compared with WT mice. Upon fasting, Prkce deletion also resulted in lower liver and plasma lipids and a smaller reduction in fat pad mass. |
|
Formal Description Interaction-ID: 57572 |
|
| Comment | Upon fasting, Prkce -/- mice were better able to maintain blood glucose levels and also exhibited lower levels of the ketone beta-hydroxybutyrate compared with WT mice. Upon fasting, Prkce deletion also resulted in lower liver and plasma lipids and a smaller reduction in fat pad mass. |
|
Formal Description Interaction-ID: 57573 |
|