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Papers In Press, published online ahead of print September 10, 2004
Albert Einstein College of Medicine, Bronx
Corresponding Author: rossetti{at}aecom.yu.edu
Leptin and insulin share some hypothalamic signaling molecules but their central administration induces different effects on hepatic glucose fluxes. Acute insulin infusion in the third cerebral ventricle (ICV) inhibits endogenous glucose production (GP) while acute leptin infusion stimulates gluconeogenesis but does not alter GP due to a compensatory decrease in glycogenolysis. Since melanocortin agonists also stimulate hepatic gluconeogenesis, here we examined whether central melanocortin blockade modifies the acute effects of leptin on GP, on gluconeogenesis, on glycogenolysis, and/or on the hepatic expression of the gluconeogenic enzymes glucose 6-phosphatase (Glc-6-Pase) and phosphoenolpyruvate carboxykinase (PEPCK). Systemic or central administration of leptin alone did not alter GP despite increasing both the rate of gluconeogenesis and the expression of Glc-6-Pase and PEPCK. When activation of the central melanocortin pathway was prevented, the effects of leptin on gluconeogenesis, Glc-6-Pase, and PEPCK were abolished and a marked suppression of glycogenolysis resulted in decreased GP. We conclude that leptin regulates hepatic glucose fluxes through a melanocortin-dependent pathway leading to stimulation of gluconeogenesis, and a melanocortin-independent pathway causing inhibition of GP and glycogenolysis.
J. Biol. Chem, 10.1074/jbc.M408665200
Submitted on July 30, 2004
Revised on September 9, 2004
Accepted on September 10, 2004
Melanocortin-independent effects of leptin on hepatic glucose fluxes
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