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绿茶多酚诱导的脂肪生成作用将脂肪细胞重塑为产热表型。

Adipogenic commitment induced by green tea polyphenols remodel adipocytes to a thermogenic phenotype.

机构信息

Department of Pharmacology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.

Interdisciplinary Post-graduate Programme in Health Sciences, Cruzeiro do Sul University, São Paulo, Brazil.

出版信息

J Nutr Biochem. 2020 Sep;83:108429. doi: 10.1016/j.jnutbio.2020.108429. Epub 2020 May 25.

DOI:10.1016/j.jnutbio.2020.108429
PMID:32563802
Abstract

The potential contribution of green tea (GT) to the development of thermogenic/beige cells have been scarcely investigated. Here we investigated if the beneficial effects of GT in the induction of thermogenic/beige adipocytes results from an initial cell commitment during adipogenesis. Male C57Bl/6 mice (3 months) were divided into 3 groups: Control (chow diet), Obese (cafeteria diet), and Obese + GT. Mice received GT gavage (500 mg/kg of BW) over 12 weeks (5 days/week), after 4 weeks of diet, totalizing 16 weeks of experimentation. GT treatment increased energy expenditure (EE) in mice fed with cafeteria-diet leading to reduced BW gain, decreased adiposity, reduced inflammation, and improving insulin sensitivity. Those phenotypes were associated with enhanced expression of oxidative, thermogenic and beige genes. GT induced a futile cycle through de novo lipogenesis activating the thermogenic pathway. Induction of beige phenotype occurs autonomously in adipocytes and involves the PPARγ/FGF21/AMPK/UCP1 pathway. Our study identified that metabolic changes caused by GT may involve the temporal expression of PPARγ promoting the induction of thermogenic cells by reprogramming initial steps of adipocyte commitment.

摘要

绿茶(GT)对产热/米色细胞的潜在贡献鲜有研究。本研究旨在探讨 GT 是否通过脂肪生成过程中的初始细胞分化来诱导产热/米色脂肪细胞。雄性 C57Bl/6 小鼠(3 月龄)分为 3 组:对照组(标准饮食)、肥胖组( cafeteria 饮食)和肥胖+GT 组。肥胖组和肥胖+GT 组给予 GT 灌胃(500mg/kgBW),每周 5 天,共 12 周,在饮食 4 周后开始实验,总实验时长为 16 周。GT 处理增加了 cafeteria 饮食喂养小鼠的能量消耗(EE),导致体重增加减少、脂肪堆积减少、炎症减轻和胰岛素敏感性提高。这些表型与氧化、产热和米色基因表达增强有关。GT 通过从头合成脂肪激活产热途径诱导无效循环。米色表型的诱导是脂肪细胞自主发生的,涉及 PPARγ/FGF21/AMPK/UCP1 途径。我们的研究表明,GT 引起的代谢变化可能涉及 PPARγ 的时间表达,通过重编程脂肪细胞分化的初始步骤来促进产热细胞的诱导。

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