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Nat Neurosci. 2005 May;8(5):566-70.

Molecular and anatomical determinants of central leptin resistance.

Author information

1
Division of Metabolism, Endocrinology and Diabetes, Department of Medicine, University of Michigan Medical School, 1150 West Medical Center Drive, Ann Arbor, Michigan 48109, USA.

Abstract

The increasing incidence of obesity in developed nations is an ever-growing challenge to health care, promoting diabetes and other diseases. The hormone leptin, which is derived from adipose tissue, regulates feeding and energy expenditure. Most forms of obesity are associated with diminished responsiveness to the appetite-suppressing effects of leptin. Here we review the mechanisms by which leptin activates intracellular signals, the roles of these signals in leptin action in vivo, and mechanisms that may attenuate leptin signaling, limiting its action in obese individuals. We highlight data regarding the expression of SOCS3 (a potential mediator of leptin resistance) in the arcuate nucleus of the hypothalamus.

PMID:
15856064
DOI:
10.1038/nn1454
[Indexed for MEDLINE]

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