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本文引用的文献

1
Association of heat production with 18F-FDG accumulation in murine brown adipose tissue after stress.应激后小鼠棕色脂肪组织中 18F-FDG 摄取与产热的关系。
J Nucl Med. 2011 Oct;52(10):1616-20. doi: 10.2967/jnumed.111.090175. Epub 2011 Sep 13.
2
Effects of burn injury, cold stress and cutaneous wound injury on the morphology and energy metabolism of murine brown adipose tissue (BAT) in vivo.烧伤、冷应激和皮肤创伤损伤对体内小鼠棕色脂肪组织（BAT）形态和能量代谢的影响。
Life Sci. 2011 Jul 18;89(3-4):78-85. doi: 10.1016/j.lfs.2011.04.014. Epub 2011 May 4.
3
Effect of simvastatin on burn-induced alterations in tissue specific glucose metabolism: implications for burn associated insulin resistance.辛伐他汀对烧伤诱导的组织特异性葡萄糖代谢改变的影响：对烧伤相关胰岛素抵抗的影响。
Int J Mol Med. 2010 Sep;26(3):311-6.
4
Brown adipose tissue--a new role in humans?棕色脂肪组织——在人类中有新作用？
Nat Rev Endocrinol. 2010 Jun;6(6):319-25. doi: 10.1038/nrendo.2010.64. Epub 2010 Apr 13.
5
The changed metabolic world with human brown adipose tissue: therapeutic visions.人类棕色脂肪组织的代谢变化世界：治疗愿景。
Cell Metab. 2010 Apr 7;11(4):268-72. doi: 10.1016/j.cmet.2010.03.007.
6
Apolipoprotein A-I possesses an anti-obesity effect associated with increase of energy expenditure and up-regulation of UCP1 in brown fat.载脂蛋白 A-I 具有抗肥胖作用，可通过增加棕色脂肪的能量消耗和上调 UCP1 来实现。
J Cell Mol Med. 2011 Apr;15(4):763-72. doi: 10.1111/j.1582-4934.2010.01045.x.
7
Brown fat as a therapy for obesity and diabetes.棕色脂肪作为肥胖和糖尿病的治疗方法。
Curr Opin Endocrinol Diabetes Obes. 2010 Apr;17(2):143-9. doi: 10.1097/MED.0b013e328337a81f.
8
BAT: a new target for human obesity?棕色脂肪组织：人类肥胖的新靶点？
Trends Pharmacol Sci. 2009 Aug;30(8):387-96. doi: 10.1016/j.tips.2009.05.003.
9
High incidence of metabolically active brown adipose tissue in healthy adult humans: effects of cold exposure and adiposity.健康成年人中代谢活跃的棕色脂肪组织发生率高：寒冷暴露和肥胖的影响。
Diabetes. 2009 Jul;58(7):1526-31. doi: 10.2337/db09-0530. Epub 2009 Apr 28.
10
Functional brown adipose tissue in healthy adults.健康成年人中的功能性棕色脂肪组织。
N Engl J Med. 2009 Apr 9;360(15):1518-25. doi: 10.1056/NEJMoa0808949.

棕色脂肪组织及其在大鼠烧伤后代谢亢进中通过靶向线粒体的肽的调节。

Brown adipose tissue and its modulation by a mitochondria-targeted peptide in rat burn injury-induced hypermetabolism.

机构信息

Shriners Hospitals for Children, Boston, 51 Blossom St., Boston, MA 02114, USA.

出版信息

Am J Physiol Endocrinol Metab. 2013 Feb 15;304(4):E331-41. doi: 10.1152/ajpendo.00098.2012. Epub 2012 Nov 20.

DOI:10.1152/ajpendo.00098.2012
PMID:23169784
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3566510/
Abstract

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.

摘要

代谢亢进是烧伤损伤的一个显著特征，而改变的线粒体功能被认为是导致这种状态的原因之一。最近，人们发现棕色脂肪组织（BAT）不仅存在于啮齿动物中，也存在于人类中，其活性与静息代谢率相关。在本报告中，我们使用大鼠烧伤模型阐明了烧伤诱导的代谢亢进与 BAT 活性之间的关系，以及线粒体靶向肽 SS31 减轻烧伤诱导的代谢亢进的可能作用。我们证明烧伤损伤诱导了肩胛间 BAT（iBAT）的形态变化。烧伤与 iBAT 的激活有关，这种作用与能量消耗的增加呈正相关。BAT 的激活与线粒体生物发生的增加以及分离的 iBAT 线粒体中 UCP1 的表达有关。此外，线粒体靶向肽 SS31 减轻了烧伤诱导的代谢亢进，同时抑制了分离的线粒体中 UCP1 的表达。我们的结果表明，BAT 通过其形态变化和 UCP1 的表达在烧伤诱导的代谢亢进中发挥重要作用。