Uncoupling protein 1 contributes to fat-reducing effect of leptin

Uncoupling protein 1 contributes to fat-reducing effect of leptin
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DOI:
10.1016/j.orcp.2007.08.001
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发表时间:
2007-12-01
影响因子:
4.3
通讯作者:
Saito, Masayuki
Saito, Masayuki
中科院分区:
医学4区
文献类型:
--
作者:
Okamatsu-Ogura, Yuko;Uozumi, Akihiro;Saito, Masayuki

文献摘要

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瘦素被认为除了减少食物摄入外,还可以通过激活棕色脂肪组织(BAT)生热作用,通过增加能量消耗来减少体脂。为了证实这一点,我们研究了瘦素对野生型(WT)小鼠全身能量消耗、BAT功能和肥胖的影响,并与缺乏BAT产热关键分子解偶联蛋白1 (UCP1)的小鼠进行了比较。腺病毒基因转移诱导的慢性高瘦素血症减少了WT和UCP1-KO小鼠的食物摄入量。与配对喂养的对照组相比,高瘦素血症的WT小鼠耗氧量增加,BAT中UCP1表达升高,白色脂肪组织(WAT)中异位UCP1诱导,体脂含量降低。在UCP1-KO小鼠中未观察到慢性高瘦素血症的这些影响。综上所述,瘦素的减脂作用不仅是由于减少了食物摄入量,而且还增加了ucp1依赖的能量消耗。(c) 2007年亚洲大洋洲肥胖研究协会。Elsevier Ltd.出版。版权所有。
Leptin is proposed to reduce body fat by increasing energy expenditure, in addition to decreasing food intake, through the activation of brown adipose tissue (BAT) thermogenesis. To confirm this, we investigated the effects of leptin on whole body energy expenditure, BAT functions and adiposity in wild-type (WT) mice, and compared with those in mice deficient in uncoupling protein 1 (UCP1), a key molecule for BAT thermogenesis. Chronic hyperleptinemia induced by adenovirus gene transfer reduced food intake in both WT and UCP1-KO mice. WT mice with hyperleptinemia, compared to pair-fed controls, showed increased oxygen consumption, elevated UCP1 expression in BAT, ectopic UCP1 induction in white adipose tissue (WAT), and reduced body fat content. These effects of chronic hyperleptinemia were not observed in UCP1-KO mice. It was concluded that the fat-reducing effect of leptin is due to not only decreased food intake, but also increased UCP1-dependent energy expenditure. (c) 2007 Asian Oceanian Association for the Study of Obesity. Published by Elsevier Ltd. All rights reserved.