CCAAT/Enhancer-binding Protein α Mediates Induction of Hepatic Phosphoenolpyruvate Carboxykinase by p38 Mitogen-activated Protein Kinase

摘要: Excessive hepatic gluconeogenesis and glucose production are important contributors to hyperglycemia in both type 1 2 diabetes. In diabetic humans animal models, elevated levels of p38 mitogen-activated protein kinase (p38) observed several tissues. Our study shows that activity is significantly livers db/db or streptozocin-induced mice. Using cultured hepatoma cells, we find activation enhances expression gluconeogenic gene phosphoenolpyruvate carboxykinase (PEPCK). Furthermore, our studies demonstrate stimulates phosphorylation CCAAT/enhancer-binding alpha (C/EBPalpha) at serine 21 increases its transactivation the context PEPCK transcription. results indicate C/EBPalpha mediates p38-stimulated transcription liver cells.