Ablation of prolactin receptor increases hepatic triglyceride accumulation
Ablation of prolactin receptor increases hepatic triglyceride accumulation
复制标题
催乳素受体的消除会增加肝脏甘油三酯的积累
DOI：
10.1016/j.bbrc.2018.03.048
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发表时间：
2018-04-06
影响因子：
3.1
通讯作者：
Gao, Ling
中科院分区：
文献类型：
--
作者：
Shao, Shanshan;Yao, Zhenyu;Gao, Ling
Increasing prevalence of non-alcoholic fatty liver disease (NAFLD) worldwide has necessitated a more thorough understanding of it and expanded the scope of research in this field. Women are more resistant to NAFLD than men despite equal exposure to major risk factors, such as obesity or hyperlipidemia. Female resistance is hormone-dependent, as evidenced by the sharp increase in NAFLD incidence in post-menopausal women who do not take hormone replacement therapy. Here, we found that the estrogen-responsive pituitary hormone prolactin (PRL), through specific PRL receptor (PRLR), down regulates hepatic triglyceride (TG) accumulation. PRL was demonstrated to significantly down-regulate hepatic TG accumulation in female mice and protect male mice from liver steatosis induced by high fat diet. Interestingly, Ad-shPRLR injected mice, whose hepatic PRLR abundance was effectively decreased at the protein levels, exhibited significantly aggravated liver steatosis. PRL could decrease the expression of stearoyl coenzyme A desaturase 1 (SCD1), the rate-limiting enzyme in the biosynthesis of monounsaturated fatty acids, in animal models and multiple hepatic cell lines. Following knockdown of PRLR, the changes to PRL-triggered SCD1 expression disappeared. Thus, PRL acted as a previously unrecognized master regulator of liver TG metabolism, indicating that modification of PRL via PRLR might serve as a potential therapeutic target for NAFLD. (C) 2018 Elsevier Inc. All rights reserved.
