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高脂饮食下雄性 mPeriod 突变小鼠的体重调节改变。

Altered body mass regulation in male mPeriod mutant mice on high-fat diet.

机构信息

Department of Neurobiology, University of Massachusetts Medical School, Worcester, Massachusetts, USA.

出版信息

Chronobiol Int. 2010 Jul;27(6):1317-28. doi: 10.3109/07420528.2010.489166.

DOI:10.3109/07420528.2010.489166
PMID:20653457
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2911971/
Abstract

The circadian clock orchestrates most physiological processes in mammals. Disruption of circadian rhythms appears to contribute to the development of obesity and metabolic syndrome. The Period genes mPer1 and mPer2, but not mPer3, are essential for core clock function in mice. To assess the impact of mPer genes on body mass regulation, mPer mutant and control mice were fed a high-fat diet. Here the authors report that male mPer1/2/3 triple-deficient mice gain significantly more body mass than wild-type controls on high-fat diet. Surprisingly, mPer3 single-deficient animals mimicked this phenotype, suggesting a previously unrecognized role for mPer3 in body mass regulation.

摘要

生物钟在哺乳动物中协调大多数生理过程。昼夜节律的破坏似乎导致肥胖和代谢综合征的发展。Period 基因 mPer1 和 mPer2,但不是 mPer3,对于小鼠的核心时钟功能是必需的。为了评估 mPer 基因对体重调节的影响,mPer 突变体和对照小鼠喂食高脂肪饮食。在这里,作者报道说,雄性 mPer1/2/3 三重缺陷型小鼠在高脂肪饮食下比野生型对照小鼠显著增加更多的体重。令人惊讶的是,mPer3 单缺陷型动物模拟了这种表型,这表明 mPer3 在体重调节中具有以前未被认识到的作用。

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Abnormal expressions of circadian-clock and circadian clock-controlled genes in the livers and kidneys of long-term, high-fat-diet-treated mice.长期高脂肪饮食处理的小鼠肝脏和肾脏中昼夜节律钟和昼夜节律钟控制基因的异常表达。
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Circadian timing of food intake contributes to weight gain.
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