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Hyperandrogenism and insulin resistance contribute to hepatic steatosis and inflammation in female rat liver.

Journal article
Authors Yuehui Zhang
Fanci Meng
Xiaoyan Sun
Xue Sun
Min Hu
Peng Cui
Edvin Vestin
Xin Li
Wei Li
Xiao-Ke Wu
John-Olov Jansson
Linus Ruijin Shao
Håkan Billig
Published in Oncotarget
Volume 9
Issue 26
Pages 18180-18197
ISSN 1949-2553
Publication year 2018
Published at Institute of Neuroscience and Physiology, Department of Physiology
Pages 18180-18197
Language en
Links dx.doi.org/10.18632/oncotarget.2447...
www.ncbi.nlm.nih.gov/entrez/query.f...
Subject categories Endocrinology, Internal medicine, Physiology

Abstract

Women with polycystic ovary syndrome (PCOS) are at high risk for nonalcoholic fatty liver disease (NAFLD). While insulin resistance is a common trait for both PCOS and NAFLD, hyperandrogenism is also considered to be a key factor contributing to PCOS, and the molecular mechanisms behind the interactions between insulin resistance and hyperandrogenism in the female liver remain largely unexplored. Using chronic treatment with insulin and/or human chorionic gonadotropin (hCG), we showed that all female rats with different treatments induced imbalance between de novo lipogenesis and mitochondrial β-oxidation via the Pparα/β-Srebp1/2-Acc1 axis, resulting in varying degrees of hepatic steatosis. Given the fact that hepatic lipid metabolism and inflammation are tightly linked processes, we found that hCG-induced hyperandrogenic rats had strongly aggravated hepatic inflammation. Further mechanistic investigations revealed that dysregulation of the IRS-PI3K-Akt signaling axis that integrated aberrant inflammatory, apoptotic and autophagic responses in the liver was strongly associated with hyperandrogenism itself or combined with insulin resistance. Additionally, we found that hCG-treated and insulin+hCG-induced rats developed visceral adipose tissue inflammation characterized by the presence of "crown like" structure and increased inflammatory gene expression. Because a more pronounced hepatic steatosis, inflammatory responses, and hepatocyte cell damage were observed in insulin+hCG-induced PCOS-like rats, our finding suggest that NAFLD seen in PCOS patients is dependent of hyperandrogenism and insulin resistance.

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