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瘦素、脂联素和抵抗素在肥胖导致睾丸间质细胞功能下降的类固醇生成基因转录调控中的作用。

Roles of leptin, adiponectin and resistin in the transcriptional regulation of steroidogenic genes contributing to decreased Leydig cells function in obesity.

作者信息

Roumaud Pauline, Martin Luc J

出版信息

Horm Mol Biol Clin Investig. 2015 Oct;24(1):25-45. doi: 10.1515/hmbci-2015-0046.

DOI:10.1515/hmbci-2015-0046
PMID:26587746
Abstract

The increase in obesity rate is a major public health issue associated with increased pathological conditions such as type 2 diabetes or cardiovascular diseases. Obesity also contributes to decreased testosterone levels in men. Indeed, the adipose tissue is an endocrine organ which produces hormones such as leptin, adiponectin and resistin. Obesity results in pathological accumulations of leptin and resistin, whereas adiponectin plasma levels are markedly reduced, all having a negative impact on testosterone synthesis. This review focuses on current knowledge related to transcriptional regulation of Leydig cells' steroidogenesis by leptin, adiponectin and resistin. We show that there are crosstalks between the regulatory mechanisms of these hormones and androgen production which may result in a dramatic negative influence on testosterone plasma levels. Indeed leptin, adiponectin and resistin can impact expression of different steroidogenic genes such as Star, Cyp11a1 or Sf1. Further investigations will be required to better define the implications of adipose derived hormones on regulation of steroidogenic genes expression within Leydig cells under physiological as well as pathological conditions.

摘要

肥胖率的上升是一个主要的公共卫生问题,与2型糖尿病或心血管疾病等病理状况增加有关。肥胖还会导致男性睾酮水平下降。事实上,脂肪组织是一个内分泌器官,可产生瘦素、脂联素和抵抗素等激素。肥胖会导致瘦素和抵抗素的病理性积累,而脂联素的血浆水平则明显降低,所有这些都会对睾酮合成产生负面影响。本综述重点关注瘦素、脂联素和抵抗素对睾丸间质细胞类固醇生成转录调控的现有知识。我们表明,这些激素的调节机制与雄激素产生之间存在相互作用,这可能会对睾酮血浆水平产生显著的负面影响。事实上,瘦素、脂联素和抵抗素会影响不同类固醇生成基因的表达,如Star、Cyp11a1或Sf1。需要进一步研究,以更好地确定脂肪衍生激素在生理和病理条件下对睾丸间质细胞内类固醇生成基因表达调控的影响。

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