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脂肪细胞产热的调控基因的最新进展。

Latest advances in the regulatory genes of adipocyte thermogenesis.

机构信息

School of Basic Medicine, Hubei University of Arts and Science, Xiangyang, China.

Scientific Research Center, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, China.

出版信息

Front Endocrinol (Lausanne). 2023 Aug 23;14:1250487. doi: 10.3389/fendo.2023.1250487. eCollection 2023.

Abstract

An energy imbalance cause obesity: more energy intake or less energy expenditure, or both. Obesity could be the origin of many metabolic disorders, such as type 2 diabetes and cardiovascular disease. UCP1 (uncoupling protein1), which is highly and exclusively expressed in the thermogenic adipocytes, including beige and brown adipocytes, can dissipate proton motive force into heat without producing ATP to increase energy expenditure. It is an attractive strategy to combat obesity and its related metabolic disorders by increasing non-shivering adipocyte thermogenesis. Adipocyte thermogenesis has recently been reported to be regulated by several new genes. This work provided novel and potential targets to activate adipocyte thermogenesis and resist obesity, such as secreted proteins ADISSP and EMC10, enzyme SSU72, etc. In this review, we have summarized the latest research on adipocyte thermogenesis regulation to shed more light on this topic.

摘要

能量失衡导致肥胖

摄入的能量过多或消耗的能量过少,或两者兼而有之。肥胖可能是许多代谢紊乱的根源,如 2 型糖尿病和心血管疾病。UCP1(解偶联蛋白 1)在产热脂肪细胞中高度且特异性表达,包括米色和棕色脂肪细胞,它可以将质子动力势耗散为热量,而不产生 ATP 来增加能量消耗。通过增加非颤抖脂肪细胞的产热来对抗肥胖及其相关代谢紊乱是一种有吸引力的策略。最近有报道称,脂肪细胞产热受到几个新基因的调节。这项工作为激活脂肪细胞产热和抵抗肥胖提供了新的潜在靶点,如分泌蛋白 ADISSP 和 EMC10、酶 SSU72 等。在这篇综述中,我们总结了脂肪细胞产热调节的最新研究进展,以期对这一课题有更深入的了解。

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