| Protein Name: | Glucose transporter-4 (P14672) |
|---|---|
| Gene Name: | SLC2A4 |
| Description: | Solute carrier family 2, facilitated glucose transporter member 4 (Glucose transporter type 4, insulin-responsive) |
| PDB ID: | |
| Protein Family: | |
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This panel provides drug-protein interaction and their ADRs along with references
| Interacting Drugs | Toxicity | Mechanism | Reference |
|---|---|---|---|
| Dexamethasone | Cushing Syndrome | Glucose metabolism in cushing#s syndrome is affected partly by a decrease of GLUT4 in the adipocytes. [ ADR Type 1 ] | Dexamethasone-induced changes in glucose transporter 4 in rat heart muscle, skeletal muscle and adipocytes |
| Glipizide | Suppression Of Hepatic Glucose Production | Glucose-induced suppression of hepatic glucose production was@ however@ more pronounced during GZ treatment ;GZ tends to normalize the activity of glycogen synthase and increases the content of GLUT 4 protein in skeletal muscle [ ADR Type 1 ] | Effects of glipizide on glucose metabolism and muscle content of the insulin-regulatable glucose transporter (GLUT 4) and glycogen synthase activity |
| Troglitazone | Beneficial For The Diabetic Heart | Troglitazone induced a dose-dependent increase in 2-deoxyglucose uptake reaching a 40-fold stimulation at 5 mumol/l@This was paralleled by a dose-dependent increase of Glucose transporter-1 (GLUT1) and GLUT4 protein expression;troglitazone exerts multiple effects on cardiomyocytes involving inhibition of PKC and regulation of Glucose transporter expression and distribution which may be beneficial for the diabetic heart and that modulation of PKC-activity could be relevant for improving insulin action in muscle tissue [ ADR Type 1 ] | Acute and chronic effects of troglitazone (CS-045) on isolated rat ventricular cardiomyocytes |
This panel provides information on drug category
| Toxicity | Source |
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