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Am J Physiol Endocrinol Metab. 2003 Oct;285(4):E685-92.

Novel concepts in insulin regulation of hepatic gluconeogenesis.

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1
Department of Endocrinology, Heinrich-Heine-University Düsseldorf, D-40225 Düsseldorf, Germany. Andreas.Barthel@uni-duesseldorf.de

Abstract

The 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.

PMID:
12959935
DOI:
10.1152/ajpendo.00253.2003
[Indexed for MEDLINE]
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