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Exp Biol Med (Maywood). 2016 Mar;241(5):449-56. doi: 10.1177/1535370215619041. Epub 2015 Dec 7.
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Obesity.肥胖症
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High selenium impairs hepatic insulin sensitivity through opposite regulation of ROS.高硒通过相反调节 ROS 损害肝脏胰岛素敏感性。
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肝细胞核因子 1b 是白色脂肪细胞分化的新型负调控因子。

Hepatocyte nuclear factor 1b is a novel negative regulator of white adipocyte differentiation.

机构信息

Department of Toxicology, Shaanxi Key Lab of Free Radical Biology and Medicine, The Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, School of Public Health, Fourth Military Medical University, Xi'an 710032, China.

出版信息

Cell Death Differ. 2017 Sep;24(9):1588-1597. doi: 10.1038/cdd.2017.85. Epub 2017 Jun 16.

DOI:10.1038/cdd.2017.85
PMID:28622294
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5563991/
Abstract

Hepatocyte nuclear factor 1b (HNF1b) is a transcription factor belonging to the HNF family. We aimed to investigate the role of HNF1b in white adipocyte differentiation. The expression of HNF1b was reduced in white adipose tissue (WAT) of both diet-induced and genetic obese mice and decreased during the process of 3T3-L1 adipocyte differentiation. Downregulation of HNF1b enhanced 3T3-L1 adipocyte differentiation and upregulation of HNF1b inhibited this process. Upregulation of HNF1b inhibited peroxisome proliferator-activated receptor γ (PPARγ) and its target gene expression, while downregulation of HNF1b increased those genes expression. Overexpression of PPARγ suppressed HNF1b upregulation-induced inhibition of adipocyte differentiation. HNF1b can directly bind with the promoter of PPARγ in 3T3-L1 cells, which was decreased after adipogenic differentiation. HNF1b promoted apoptotic and autophagic cell death in early differentiated adipocytes through regulation of cell cycle progress and cell death-related factors, and thus inhibited the process of mitotic clonal expansion (MCE). HNF1b acted as an antioxidant regulator through regulating various antioxidant enzymes via binding with antioxidant response element. Oxidant treatment suppressed HNF1b upregulation-induced inhibition of adipocyte differentiation. Overall, our results suggest that HNF1b is a novel negative regulator of adipocyte differentiation through regulation of PPARγ signaling, MCE and redox state.

摘要

肝细胞核因子 1b（HNF1b）是一种属于 HNF 家族的转录因子。我们旨在研究 HNF1b 在白色脂肪细胞分化中的作用。在饮食诱导和遗传肥胖的小鼠的白色脂肪组织（WAT）中，HNF1b 的表达减少，并且在 3T3-L1 脂肪细胞分化过程中减少。下调 HNF1b 增强了 3T3-L1 脂肪细胞分化，而上调 HNF1b 则抑制了这一过程。上调 HNF1b 抑制过氧化物酶体增殖物激活受体 γ（PPARγ）及其靶基因的表达，而下调 HNF1b 则增加了这些基因的表达。过表达 PPARγ 抑制了 HNF1b 上调诱导的脂肪细胞分化抑制。HNF1b 可以直接与 3T3-L1 细胞中 PPARγ 的启动子结合，在脂肪生成分化后这种结合减少。HNF1b 通过调节细胞周期进程和细胞死亡相关因子，促进早期分化的脂肪细胞发生凋亡和自噬性细胞死亡，从而抑制有丝分裂克隆扩增（MCE）过程。HNF1b 通过与抗氧化反应元件结合，调节各种抗氧化酶，作为抗氧化调节剂。氧化剂处理抑制了 HNF1b 上调诱导的脂肪细胞分化抑制。总之，我们的研究结果表明，HNF1b 通过调节 PPARγ 信号、MCE 和氧化还原状态，是脂肪细胞分化的一种新型负调控因子。