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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Targeted deletion of thioesterase superfamily member 1 promotes energy expenditure and protects against obesity and insulin resistance
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Targeted deletion of thioesterase superfamily member 1 promotes energy expenditure and protects against obesity and insulin resistance

机译：硫酯酶超家族成员1的有针对性的删除促进能源消耗，并防止肥胖和胰岛素抵抗

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摘要

Mammalian acyl-CoA thioesterases (Acots) catalyze the hydrolysis of fatty acyl-CoAs to form free fatty acids plus CoA, but their metabolic functions remain undefined. Thioesterase superfamily member 1 (Themi; synonyms Acot11, StarD14, and brown fat inducible thioesterase) is a long-chain fatty acyl-CoA thioesterase that is highly expressed in brown adipose tissue and is regulated by both ambient temperature and food consumption. Here we show that Them1~(-/-) mice were resistant to diet-induced obesity despite greater food consumption. Them1~(-/-) mice exhibited increased O_2 consumption and heat production, which were accompanied by increased rates of fatty acid oxidation in brown adipose tissue and up-regulation of genes that promote energy expenditure. Them1~(-/-) mice were also protected against diet-induced inflammation in white adipose tissue, as well as hepatic steatosis, and demonstrated improved glucose homeostasis. The absence of Themi expression in vivo and in cell culture led to markedly attenuated diet- or chemically induced endoplasmic reticulum stress responses, providing a mechanism by which Themi deficiency protects against insulin resistance and lipid deposition. Taken together, these data suggest that Themi functions to decrease energy consumption and conserve calories. In the setting of nutritional excess, the overproduction of free fatty acids by Themi provokes insulin resistance that is associated with inflammation and endoplasmic reticulum stress.
机译：哺乳动物酰基辅酶A硫酯酶（Acots）催化脂肪酰基辅酶A水解，形成游离脂肪酸和辅酶A，但它们的代谢功能仍然不确定。硫酯酶超家族成员1（Themi;同义词Acot11，StarD14和棕色脂肪可诱导的硫酯酶）是一种长链脂肪酰基-CoA硫酯酶，在棕色脂肪组织中高度表达，并受环境温度和食物消耗的调节。在这里，我们显示Them1〜（-/-）小鼠尽管进食较多，但仍能抵抗饮食诱发的肥胖。 m1〜（-/-）小鼠表现出增加的O_2消耗和热量产生，并伴随着棕色脂肪组织中脂肪酸氧化速率的增加以及促进能量消耗的基因的上调。他们还保护了小鼠（-/-）免受饮食诱导的白色脂肪组织炎症以及肝脂肪变性，并改善了葡萄糖的体内稳态。在体内和细胞培养物中不存在Themi表达导致饮食或化学诱导的内质网应激反应明显减弱，从而提供了Themi缺乏症抵抗胰岛素抵抗和脂质沉积的机制。综上所述，这些数据表明，西米具有减少能量消耗和节省卡路里的功能。在营养过剩的情况下，Themi过量生产游离脂肪酸会引起胰岛素抵抗，而胰岛素抵抗与炎症和内质网应激有关。

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    Yongzhao Zhang; Yingxia Li; Michele W. Niepel; Yuki Kawano; Shuxin Han; Sihao Liu; Alessandro Marsili; P. Reed Larsen; Chih-Hao Lee; David E. Cohen;

  • 作者单位

    Department of Medicine, B.righam and Women's Hospital, Harvard Medical School, Boston, MA 02115;

    Department of Medicine, B.righam and Women's Hospital, Harvard Medical School, Boston, MA 02115;

    Department of Medicine, B.righam and Women's Hospital, Harvard Medical School, Boston, MA 02115;

    Department of Medicine, B.righam and Women's Hospital, Harvard Medical School, Boston, MA 02115;

    Department of Medicine, B.righam and Women's Hospital, Harvard Medical School, Boston, MA 02115;

    Department of Genetics and Complex Diseases, Division of Biological Sciences, Harvard School of Public Health, Boston, MA 02115;

    Department of Medicine, B.righam and Women's Hospital, Harvard Medical School, Boston, MA 02115;

    Department of Medicine, B.righam and Women's Hospital, Harvard Medical School, Boston, MA 02115;

    Department of Genetics and Complex Diseases, Division of Biological Sciences, Harvard School of Public Health, Boston, MA 02115;

    Department of Medicine, B.righam and Women's Hospital, Harvard Medical School, Boston, MA 02115;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    thermogenesis; liver; diabetes;

    机译：生热肝;糖尿病;

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