Literature DB >> 25720568

Hepatic estrogen receptor α improves hepatosteatosis through upregulation of small heterodimer partner.

Xiaolin Wang1, Yan Lu1, E Wang1, Zhijian Zhang1, Xuelian Xiong1, Huijie Zhang2, Jieli Lu1, Sheng Zheng1, Jian Yang1, Xuefeng Xia3, Shuyu Yang4, Xiaoying Li5.   

Abstract

BACKGROUND & AIMS: Estrogen participates in the control of energy homeostasis and lipid metabolism. However the role of hepatic estrogen receptor α (ERα) in triglyceride (TG) homeostasis remains poorly understood. This study aims to investigate the roles of estrogen and ERα in the regulation of hepatic TG metabolism.
METHODS: Liver TG metabolism was analyzed in female mice with ovariectomy or tamoxifen treatment, and in hepatic ERα knockdown or overexpression. Phenotypes and expression of genes were compared in male and female mice with farnesoid X receptor deficiency. The mechanism of ERα in the regulation of small heterodimer partner (SHP) expression was further investigated.
RESULTS: Female mice receiving ovariectomy or tamoxifen treatment exhibited hepatic TG accumulation. Ablation of ERα using adenoviral shRNA markedly increased hepatic TG accumulation, while overexpression of ERα ameliorated hepatosteatosis in obese mice. At the molecular level, estrogen upregulated hepatic SHP expression through binding to its proximal promoter. In addition, the roles of estrogen were largely blunted in mice with SHP deficiency.
CONCLUSION: These findings reveal a novel role of estrogen in improving hepatosteatosis through upregulation of SHP expression.
Copyright © 2015 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.

Entities:  

Keywords:  ERα; Estrogen; FXR; Hepatosteatosis; SHP

Mesh:

Substances:

Year:  2015        PMID: 25720568     DOI: 10.1016/j.jhep.2015.02.029

Source DB:  PubMed          Journal:  J Hepatol        ISSN: 0168-8278            Impact factor:   25.083


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