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迈向对适应性产热的分子理解。

Towards a molecular understanding of adaptive thermogenesis.

作者信息

Lowell B B, Spiegelman B M

机构信息

Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA.

出版信息

Nature. 2000 Apr 6;404(6778):652-60. doi: 10.1038/35007527.

Abstract

Obesity results when energy intake exceeds energy expenditure. Naturally occurring genetic mutations, as well as ablative lesions, have shown that the brain regulates both aspects of energy balance and that abnormalities in energy expenditure contribute to the development of obesity. Energy can be expended by performing work or producing heat (thermogenesis). Adaptive thermogenesis, or the regulated production of heat, is influenced by environmental temperature and diet. Mitochondria, the organelles that convert food to carbon dioxide, water and ATP, are fundamental in mediating effects on energy dissipation. Recently, there have been significant advances in understanding the molecular regulation of energy expenditure in mitochondria and the mechanisms of transcriptional control of mitochondrial genes. Here we explore these developments in relation to classical physiological views of adaptive thermogenesis.

摘要

当能量摄入超过能量消耗时,就会导致肥胖。自然发生的基因突变以及消融性病变表明,大脑调节能量平衡的两个方面,且能量消耗异常会导致肥胖的发生。能量可以通过做功或产热(生热作用)来消耗。适应性生热作用,即热量的调节产生,受环境温度和饮食的影响。线粒体是将食物转化为二氧化碳、水和三磷酸腺苷的细胞器,在介导对能量消散的影响方面至关重要。最近,在理解线粒体能量消耗的分子调节以及线粒体基因转录控制机制方面取得了重大进展。在此,我们结合适应性生热作用的经典生理学观点来探讨这些进展。

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