罗格列酮增强褐色脂肪形成过程中GPR43的表达并受PPARγ/RXR异源二聚化控制

IF 3.5 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL PPAR Research Pub Date : 2018-05-16 eCollection Date: 2018-01-01 DOI:10.1155/2018/1051074
Jiamiao Hu, Arong Zhou, Peter C K Cheung, Baodong Zheng, Shaoxiao Zeng, Shaoling Lin
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引用次数: 10

摘要

GPR43是一种识别短链脂肪酸的g蛋白偶联受体,已被报道参与白色脂肪细胞的许多生物学功能,如脂肪形成和脂肪分解。然而,GPR43在棕色脂肪细胞中的功能作用尚不清楚。在这项研究中,我们研究了PPARγ激动剂罗格列酮对褐色脂肪形成中GPR43表达的影响。结果表明,GPR43在棕色脂肪细胞分化后期表达,罗格列酮可进一步增强GPR43的表达。研究发现,PPARγ/RXR异源二聚化是罗格列酮增强GPR43表达的关键转录因子。综上所述,这些结果表明GPR43水平可能在棕色脂肪细胞分化过程中受到ppar γ激活事件的调节,并反映了棕色脂肪细胞的脂肪形成状态。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Expression of GPR43 in Brown Adipogenesis Is Enhanced by Rosiglitazone and Controlled by PPARγ/RXR Heterodimerization.

GPR43, a G-protein coupled receptor recognizing short-chain fatty acids, has been reported to participate in many biological functions of white adipocytes, such as adipogenesis and lipolysis. However, the functional role of GPR43 in brown adipocytes is still not clear. In this study, we investigated the effects of the PPARγ agonist rosiglitazone on GPR43 expression in brown adipogenesis. The results demonstrated that GPR43 was expressed during the late phase of brown adipocyte differentiation, which could be further augmented by adipogenic agent rosiglitazone treatment. The PPARγ/RXR heterodimerization was found to be the key transcription factor for this enhancing effect of rosiglitazone on GPR43 expression. Taken together, these results suggested GPR43 levels might be regulated by PPARγ-activated events during brown adipocytes differentiation and reflect the adipogenesis status of brown adipocytes.

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来源期刊
PPAR Research
PPAR Research MEDICINE, RESEARCH & EXPERIMENTAL-
CiteScore
6.20
自引率
3.40%
发文量
17
审稿时长
12 months
期刊介绍: PPAR Research is a peer-reviewed, Open Access journal that publishes original research and review articles on advances in basic research focusing on mechanisms involved in the activation of peroxisome proliferator-activated receptors (PPARs), as well as their role in the regulation of cellular differentiation, development, energy homeostasis and metabolic function. The journal also welcomes preclinical and clinical trials of drugs that can modulate PPAR activity, with a view to treating chronic diseases and disorders such as dyslipidemia, diabetes, adipocyte differentiation, inflammation, cancer, lung diseases, neurodegenerative disorders, and obesity.
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