EPIGENETIC CONTROL AND THE CIRCADIAN CLOCK: LINKING METABOLISM TO NEURONAL RESPONSES

被引:67
|
作者
Orozco-Solis, R. [1 ]
Sassone-Corsi, P. [1 ]
机构
[1] Univ Calif Irvine, Dept Biol Chem, Ctr Epigenet & Metab, Unite INSERM 904, Irvine, CA 92697 USA
关键词
epigenetic mechanism; clock; SIRT1; metabolism; social zeitgebers; nutrients; DORSOMEDIAL HYPOTHALAMIC NUCLEUS; REGULATES FOOD-INTAKE; SUPRACHIASMATIC NUCLEUS; GENE-EXPRESSION; NERVOUS-SYSTEM; ENERGY-BALANCE; HISTONE ACETYLTRANSFERASE; LOCOMOTOR-ACTIVITY; SIRT1; DEACETYLASE; PERIPHERAL CLOCKS;
D O I
10.1016/j.neuroscience.2014.01.043
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Experimental and epidemiological evidence reveal the profound influence that industrialized modern society has imposed on human social habits and physiology during the past 50 years. This drastic change in life-style is thought to be one of the main causes of modern diseases including obesity, type 2 diabetes, mental illness such as depression, sleep disorders, and certain types of cancer. These disorders have been associated to disruption of the circadian clock, an intrinsic time-keeper molecular system present in virtually all cells and tissues. The circadian clock is a key element in homeostatic regulation by controlling a large array of genes implicated in cellular metabolism. Importantly, intimate links between epigenetic regulation and the circadian clock exist and are likely to prominently contribute to the plasticity of the response to the environment. In this review, we summarize some experimental and epidemiological evidence showing how environmental factors such as stress, drugs of abuse and changes in circadian habits, interact through different brain areas to modulate the endogenous clock. Furthermore we point out the pivotal role of the deacetylase silent mating-type information regulation 2 homolog 1 (SIRT1) as a molecular effector of the environment in shaping the circadian epigenetic landscape. This article is part of a Special Issue entitled: Epigenetics in Brain Function. Published by Elsevier Ltd. on behalf of IBRO.
引用
收藏
页码:76 / 87
页数:12
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