Circadian rhythms in adipose tissue: an update
Circadian rhythms in adipose tissue: an update
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DOI：
10.1097/mco.0b013e32834ad94b
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发表时间：
2011-11-01
影响因子：
3.1
通讯作者：
Bunnell, Bruce A.
中科院分区：
文献类型：
--
作者：
Gimble, Jeffrey M.;Sutton, Gregory M.;Bunnell, Bruce A.
综述的目的在过去的十年里，基础科学、临床和流行病学研究积累了大量证据，将昼夜节律机制与脂肪组织生物学及其相关的合并症、糖尿病、代谢综合征和肥胖联系起来。这篇综述强调了最近在体外和体内的发现从小鼠，人类和模式生物study.Recent findingsHigh-fat diets衰减昼夜节律机制在小鼠脂肪depots和这些影响似乎是由于肥胖，而不是高血糖症。昼夜节律调节基因如AMPK 1和Akt Turnin的缺失改变了脂肪组织的昼夜节律生物学。与小鼠不同，人类脂肪组织中的昼夜节律基因振荡似乎与BMI和糖尿病状态无关，这表明昼夜节律机制的变化发生在物种之间。在这一新兴领域的未来发展方向的线索来自研究的冬眠和麻痹状态的哺乳动物和感染模型，涉及果蝇代谢器官或'脂肪body'. SummaryThere是一个越来越多的共识，昼夜节律和代谢密切调节脂肪组织和外周代谢器官。虽然中枢机制是至关重要的，自主时钟存在于脂肪细胞本身。未来的昼夜节律进展可能来自脂肪组织特异性基因缺失的研究。
Purpose of reviewOver the past decade, evidence has accumulated from basic science, clinical and epidemiological studies linking circadian mechanisms to adipose tissue biology and its related comorbidities, diabetes, metabolic syndrome and obesity. This review highlights recent in-vitro and in-vivo findings from murine, human and model organism studies.Recent findingsHigh-fat diets attenuate circadian mechanisms in murine adipose depots and these effects appear to be due to obesity rather than hyperglycemia. Deletion of circadian regulatory genes such as AMPK1 and nocturnin alter the circadian biology of adipose tissue. Unlike the mouse, circadian gene oscillation in human adipose tissue appears to be independent of BMI and diabetes status, suggesting that circadian mechanistic variation occurs across species. Clues for future directions in this emerging field come from studies of the hibernation and torpor state in mammals and infection models involving the Drosophila metabolic organ or 'fat body'.SummaryThere is a growing consensus that circadian rhythms and metabolism are tightly regulated in adipose tissue and peripheral metabolic organs. Although central mechanisms are critical, autonomous clocks exist within the adipocytes themselves. Future circadian advances are likely to result from the studies of adipose tissue-specific gene deletions.