Division of Metabolism, Endocrinology and Diabetes, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Trends Endocrinol Metab. 2010 Nov;21(11):643-51. doi: 10.1016/j.tem.2010.08.002. Epub 2010 Sep 16.
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.
由于瘦素可降低食物摄入量和体重，因此人们普遍将瘦素水平升高与肥胖并存解释为“瘦素抵抗”的证据。事实上，肥胖会促进许多削弱瘦素信号的细胞过程（这里称为“细胞性瘦素抵抗”），并放大遗传和环境因素引起的体重增加程度。然而，正如通常使用的那样，“瘦素抵抗”一词包含了一系列在潜在机制和病理生理学意义上不同的现象。此外，肥胖引起的细胞性瘦素抵抗使区分导致体重增加的机制与由此产生的机制变得复杂。我们提出了一种解决这些问题的框架，并为未来的研究提供了重要途径。
