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Circadian Dysfunction Induces Leptin Resistance in Mice

机译：昼夜节律紊乱诱导小鼠瘦素抵抗。

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Circadian disruption is associated with obesity, implicating the central clock in body weight control. Our comprehensive screen of wild-type and three circadian mutant mouse models, with or without chronic jet lag, shows that distinct genetic and physiologic interventions differentially disrupt overall energy homeostasis and Leptin signaling. We found that BMAL1/CLOCK generates circadian rhythm of C/EBP alpha-mediated leptin transcription in adipose. Per and Cry mutant mice show similar disruption of peripheral clock and deregulation of leptin in fat, but opposite body weight and composition phenotypes that correlate with their distinct patterns of POMC neuron deregulation in the arcuate nucleus. Chronic jet lag is sufficient to disrupt the endogenous adipose clock and also induce central Leptin resistance in wild-type mice. Thus, coupling of the central and peripheral clocks controls Leptin endocrine feedback homeostasis. We propose that Leptin resistance, a hallmark of obesity in humans, plays a key role in circadian dysfunction-induced obesity and metabolic syndromes.
机译：昼夜节律紊乱与肥胖有关，这牵涉到体重控制中的中央时钟。我们对野生型和三个昼夜节律突变小鼠模型（有或没有慢性时差反应）进行的全面筛选显示，不同的遗传和生理干预差异性地破坏了总体能量稳态和瘦素信号传导。我们发现BMAL1 / CLOCK在脂肪中产生C / EBPα介导的瘦素转录的昼夜节律。 Per和Cry突变小鼠在脂肪中显示出类似的外周时钟破坏和瘦素失调的现象，但是体重和组成表型却相反，这与弓形核中POMC神经元失调的独特模式有关。慢性时差反应足以破坏内源性脂肪时钟，并在野生型小鼠中引起中枢瘦素抵抗。因此，中央时钟和外围时钟的耦合控制了瘦素内分泌反馈的体内平衡。我们提出，瘦素抵抗是人类肥胖的标志，在昼夜节律紊乱引起的肥胖和代谢综合征中起关键作用。

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