Obesity and leptin resistance: distinguishing cause from effect.

[Mike Bikov]

Trends Endocrinol Metab. 2010 Sep 14. [Epub ahead of print]
Obesity and leptin resistance: distinguishing cause from effect.

Myers MG Jr, Leibel RL, Seeley RJ, Schwartz MW.

Division of Metabolism, Endocrinology and Diabetes, Department of Internal Medicine and Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA.
Abstract

Because leptin reduces food intake and body weight, the coexistence of elevated leptin levels with obesity is widely interpreted as evidence of 'leptin resistance.' Indeed, obesity promotes a number of cellular processes that attenuate leptin signaling (referred to here as 'cellular leptin resistance') and amplify the extent of weight gain induced by genetic and environmental factors. As commonly used, however, the term 'leptin resistance' embraces a range of phenomena that are distinct in underlying mechanisms and pathophysiological implications. Moreover, the induction of cellular leptin resistance by obesity complicates efforts to distinguish the mechanisms that predispose to weight gain from those that result from it. We suggest a framework for approaching these issues and important avenues for future investigation.​

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