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lüll Novel concepts in insulin regulation of hepatic gluconeogenesis Barthel A; Schmoll DAm J Physiol Endocrinol Metab 2003[Oct]; 285 (4): E685-92The regulation of hepatic gluconeogenesis is an important process in the adjustment of the blood glucose level, and pathological changes in the glucose production of the liver are a central characteristic in type 2 diabetes. The pharmacological intervention in signaling events that regulate the expression of the key gluconeogenic enzymes phosphoenolpyruvate carboxykinase (PEPCK) and the catalytic subunit glucose-6-phosphatase (G-6-Pase) is regarded as a potential strategy for the treatment of metabolic aberrations associated with this disease. However, such intervention requires a detailed understanding of the molecular mechanisms involved in the regulation of this process. Glucagon and glucocorticoids are known to increase hepatic gluconeogenesis by inducing the expression of PEPCK and G-6-Pase. The coactivator protein PGC-1 has been identified as an important mediator of this regulation. In contrast, insulin is known to suppress both PEPCK and G-6-Pase gene expression by the activation of PI 3-kinase. However, PI 3-kinase-independent pathways can also lead to the inhibition of gluconeogenic enzymes. This review focuses on signaling mechanisms and nuclear events that transduce the regulation of gluconeogenic enzymes.|Animals[MESH]|Diabetes Mellitus, Type 2/*metabolism[MESH]|Genes, Regulator/physiology[MESH]|Gluconeogenesis/*physiology[MESH]|Glucose-6-Phosphatase/*metabolism[MESH]|Homeostasis/*physiology[MESH]|Humans[MESH]|Insulin/*metabolism[MESH]|Liver/enzymology/*metabolism/physiology[MESH]|Multienzyme Complexes[MESH]|Phosphoenolpyruvate Carboxykinase (ATP)/*metabolism[MESH] |