Obesity and metabolic syndrome in circadian Clock mutant mice
Obesity and metabolic syndrome in circadian Clock mutant mice
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DOI：
10.1126/science.1108750
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发表时间：
2005-05-13
期刊：
影响因子：
56.9
通讯作者：
Bass, J
中科院分区：
文献类型：
--
作者：
Turek, FW;Joshu, C;Bass, J
CLOCK转录因子是下丘脑视交叉上核起搏神经元内分子生物钟的关键组成部分。我们发现，纯合子Clock突变小鼠的昼夜摄食节律大大减弱，贪食和肥胖，并出现高瘦素血症、高脂血症、肝脂肪变性、高血糖和低胰岛素血症的代谢综合征。在Clock突变小鼠中，编码与能量平衡相关的所选下丘脑肽的转录物的表达减弱。这些结果表明，生物钟基因网络在哺乳动物的能量平衡中起着重要的作用。
The CLOCK transcription factor is a key component of the molecular circadian clock within pacemaker neurons of the hypothalamic suprachiasmatic nucleus. We found that homozygous Clock mutant mice have a greatly attenuated diurnal feeding rhythm, are hyperphagic and obese, and develop a metabolic syndrome of hyperleptinemia, hyperlipidemia, hepatic steatosis, hyperglycemia, and hypoinsulinemia. Expression of transcripts encoding selected hypothalamic peptides associated with energy balance was attenuated in the Clock mutant mice. These results suggest that the circadian clock gene network plays an important rote in mammalian energy balance.