矢车菊素-3-葡萄糖苷通过激活Prdm16基因调控棕色脂肪组织中 的表达。 （原文中“ ”处内容缺失，翻译时保留原样）
Cyanidin-3--glucoside Regulates the Expression of in Brown Adipose Tissue by Activating Prdm16 Gene.
作者信息
Han Suping, Yang Yafan, Lu Yanan, Guo Jielong, Han Xue, Gao Yunxiao, Huang Weidong, You Yilin, Zhan Jicheng
机构信息
Beijing Key Laboratory of Viticulture and Enology, College of Food Science and Nutritional Engineering, China Agricultural University, Tsinghua East Road 17, Beijing 100083, China.
School of Biomedicine, Beijing City University, Beijing 100094, China.
出版信息
Antioxidants (Basel). 2021 Dec 14;10(12):1986. doi: 10.3390/antiox10121986.
(1) Background: Brown adipose tissue (BAT) burns energy to produce heat. Cyanidin-3--glucoside (C3G) can then enhance the thermogenic ability of BAT in vivo. However, the mechanism by which C3G regulates Ucp1 protein expression remains unclear. (2) Methods: In this study, C3H10T12 brown adipose cells and db/db mice and mice with high-fat, high-fructose, diet-induced obesity were used as the model to explore the effect of C3G on the expression of the gene. Furthermore, the 293T cell line was used for an in vitro cell transgene, a double luciferase reporting system, and yeast single hybridization to explore the mechanism of C3G in regulating Ucp1 protein. (3) Results: we identified that, under the influence of C3G, Prdm16 directly binds to the -500 to -150 bp promoter region of to activate its transcription and, thus, facilitate BAT programming. (4) Conclusions: This study clarified the mechanism by which C3G regulates the expression of the gene of brown fat to a certain extent.
(1) 背景：棕色脂肪组织（BAT）通过燃烧能量产生热量。花青素-3-葡萄糖苷（C3G）可增强BAT在体内的产热能力。然而，C3G调节解偶联蛋白1（Ucp1）蛋白表达的机制尚不清楚。(2) 方法：在本研究中，以C3H10T12棕色脂肪细胞、db/db小鼠以及高脂高糖饮食诱导肥胖的小鼠作为模型，探究C3G对该基因表达的影响。此外，利用293T细胞系进行体外细胞转基因、双荧光素酶报告系统以及酵母单杂交实验，以探究C3G调节Ucp1蛋白的机制。(3) 结果：我们发现，在C3G的影响下，PR结构域蛋白16（Prdm16）直接结合到Ucp1基因-500至-150 bp的启动子区域以激活其转录，从而促进棕色脂肪组织编程。(4) 结论：本研究在一定程度上阐明了C3G调节棕色脂肪Ucp1基因表达的机制。
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