Ablation of prolactin receptor increases hepatic triglyceride accumulation.

Ablation of prolactin receptor increases hepatic triglyceride accumulation. Biochem Biophys Res Commun. 2018 Mar 07;: Authors: Shao S, Yao Z, Lu J, Song Y, He Z, Yu C, Zhou X, Zhao L, Zhao J, Gao L Abstract 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 d...
Source: Biochemical and Biophysical Research communications - Category: Biochemistry Authors: Tags: Biochem Biophys Res Commun Source Type: research