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脂肪组织的生物钟:更新。

Circadian rhythms in adipose tissue: an update.

机构信息

Stem Cell Biology Laboratory, Pennington Biomedical Research Center, Baton Rouge, LA 70808, USA.

出版信息

Curr Opin Clin Nutr Metab Care. 2011 Nov;14(6):554-61. doi: 10.1097/MCO.0b013e32834ad94b.

Abstract

PURPOSE OF REVIEW

Over 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 FINDINGS

High-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'.

SUMMARY

There 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.

摘要

目的综述

在过去的十年中,越来越多的证据表明,昼夜节律机制与脂肪组织生物学及其相关的合并症(如糖尿病、代谢综合征和肥胖)有关。这篇综述强调了最近来自啮齿动物、人类和模式生物研究的体外和体内发现。

最近的发现

高脂肪饮食会削弱啮齿动物脂肪组织中的昼夜节律机制,这些影响似乎是由于肥胖而不是高血糖引起的。昼夜节律调节基因如 AMPK1 和 nocturnin 的缺失会改变脂肪组织的昼夜生物学。与小鼠不同,人类脂肪组织中的昼夜基因振荡似乎与 BMI 和糖尿病状态无关,这表明昼夜机制在不同物种之间存在差异。从哺乳动物的冬眠和蛰伏状态以及涉及果蝇代谢器官或“脂肪体”的感染模型的研究中,可以为这一新兴领域的未来方向提供线索。

总结

越来越多的共识认为,昼夜节律和代谢在脂肪组织和外周代谢器官中受到严格调节。虽然中枢机制是关键的,但脂肪细胞本身也存在自主时钟。未来的昼夜节律进展可能来自于脂肪组织特异性基因缺失的研究。

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