Brown adipose tissue and its modulation by a mitochondria-targeted peptide in rat burn injury-induced hypermetabolism
Brown adipose tissue and its modulation by a mitochondria-targeted peptide in rat burn injury-induced hypermetabolism
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DOI：
10.1152/ajpendo.00098.2012
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发表时间：
2013-02-01
影响因子：
5.1
通讯作者：
Fischman, Alan J.
中科院分区：
文献类型：
--
作者：
Yo, Kikuo;Yu, Yong-Ming;Fischman, Alan J.
Yo K，Yu Ym，赵G，Bonab AA，Aikawa N，Tompkins RG，Fischman AJ。烧伤大鼠棕色脂肪组织及其线粒体靶向多肽的调节作用。Am J生理学内分泌Metab 304：E331-E341,2013。2012年11月20日首次发表；doi:10.1152/ajpendo.00098.2012.-Hypermetabolism是烧伤的一个显著特征，线粒体功能改变被认为是导致这种状态的原因之一。近年来发现，棕色脂肪组织(BAT)不仅存在于啮齿动物体内，也存在于人类体内，其活性与静息代谢率有关。在本报告中，我们通过大鼠烧伤模型，阐明了烧伤高代谢与BAT活性的关系以及线粒体靶向多肽SS31在减轻烧伤高代谢中的可能作用。我们证明烧伤可以引起肩峰间蝙蝠(IBAT)的形态改变。烧伤与iBAT激活有关，且这种作用与能量消耗增加呈正相关。BAT的激活与线粒体生物发生的增强以及分离的iBAT线粒体中UCP1的表达有关。此外，线粒体靶向多肽SS31可减轻烧伤所致的高代谢，同时抑制UCP1在分离线粒体中的表达。结果提示，BAT通过其形态变化和UCP1的表达在烧伤所致的高代谢中起重要作用。
Yo K, Yu YM, Zhao G, Bonab AA, Aikawa N, Tompkins RG, Fischman AJ. Brown adipose tissue and its modulation by a mitochondria-targeted peptide in rat burn injury-induced hypermetabolism. Am J Physiol Endocrinol Metab 304: E331-E341, 2013. First published November 20, 2012; doi:10.1152/ajpendo.00098.2012.-Hypermetabolism is a prominent feature of burn injury, and altered mitochondria function is presumed to contribute to this state. Recently, brown adipose tissue (BAT) was found to be present not only in rodents but also in humans, and its activity is associated with resting metabolic rate. In this report, we elucidate the relationship between burn injury-induced hypermetabolism and BAT activity and the possible role of the mitochondria-targeted peptide SS31 in attenuating burn injury-induced hypermetabolism by using a rat burn injury model. We demonstrate that burn injury induces morphological changes in interscapular BAT (iBAT). Burn injury was associated with iBAT activation, and this effect was positively correlated with increased energy expenditure. BAT activation was associated with augmentation of mitochondria biogenesis, and UCP1 expression in the isolated iBAT mitochondria. In addition, the mitochondria-targeted peptide SS31 attenuated burn injury-induced hypermetabolism, which was accompanied by suppression of UCP1 expression in isolated mitochondria. Our results suggest that BAT plays an important role in burn injury-induced hypermetabolism through its morphological changes and expression of UCP1.