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在转录相互作用分析中,睾酮抑制过氧化物酶体增殖物激活受体γ的活性。

Testosterone inhibits the activity of peroxisome proliferator-activated receptor gamma in a transcriptional transaction assay.

作者信息

Du J, Zhang L, Wang Z

机构信息

Protein Science Key Laboratory of the Ministry of Education, Department of Biological Sciences and Biotechnology, School of Medicine, Tsinghua University, Beijing, PR China.

出版信息

Pharmazie. 2009 Oct;64(10):692-3.

Abstract

Emerging evidences suggest that testosterone is an important regulator of body fat mass in men. However, the mechanism underlying the regulation of body composition by testosterone is not well understood. The paper demonstrates testosterone inhibited the activity of peroxisome proliferator-activated receptor gamma (PPARgamma), which controls the adipogenic differentiation and lipid metabolism. Pre-inhibition of androgen receptor did not influence the inhibition of PPARgamma activity by testosterone. Moreover, pre-treatment with testosterone attenuated the insulin-induced up-regulation of PPARgamma activity. These results provide a novel mechanism for the effect of testosterone on fat mass control.

摘要

新出现的证据表明,睾酮是男性体内脂肪量的重要调节因子。然而,睾酮调节身体成分的潜在机制尚未完全明确。该论文表明,睾酮抑制了过氧化物酶体增殖物激活受体γ(PPARγ)的活性,而PPARγ控制着脂肪生成分化和脂质代谢。预先抑制雄激素受体并不影响睾酮对PPARγ活性的抑制作用。此外,睾酮预处理减弱了胰岛素诱导的PPARγ活性上调。这些结果为睾酮对脂肪量控制的作用提供了一种新机制。

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