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This version published online on January 17, 2008
Molecular Endocrinology, doi:10.1210/me.2007-0529
Molecular Endocrinology Vol. 0, No. 2008 200705291-
doi:10.1210/me.2007-0529
Copyright © 2008 by the Endocrine Society.
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Submitted on November 27, 2007
Accepted on January 9, 2008

Adipokines and the Peripheral and Neural Control of Energy Balance

Rexford S. Ahima* and Mitchell A. Lazar

Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Pennsylvania School of Medicine, and the Institute for Diabetes, Obesity and Metabolism, University of Pennsylvania, Philadelphia, Pennsylvania

* To whom correspondence should be addressed. E-mail: ahima{at}mail.med.upenn.edu.

Adipokines are secreted by adipose tissue and control various physiological systems. Low leptin levels during fasting stimulate feeding, reduce energy expenditure, and modulate neuroendocrine and immune function to conserve energy stores. On the other hand, rising leptin levels in the overfed state prevent weight gain by inhibiting food intake and increasing energy expenditure. These actions are mediated by neuronal circuits in the hypothalamus and brainstem. Leptin also controls glucose and lipid metabolism by targeting enzymes such as AMP-activated protein kinase (AMPK) and stearoyl-CoA desaturase-1 in liver and muscle. Likewise, adiponectin and resistin control energy balance and insulin sensitivity via central and peripheral targets. As highlighted in this review, there are distinct as well as common signaling pathways for adipokines. Understanding adipokine signaling in the brain and other organs will provide insights into the pathogenesis and treatment of obesity, diabetes, and various metabolic disorders.




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