ArticleEndocrine2024
Androgens exacerbate hepatic triglyceride accumulation in rats with polycystic ovary syndrome by downregulating MTTP expression.
Article in Endocrine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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Who cites it
3 citing papers in PubMed.
- The central role of hyperandrogenism in driving metabolic dysfunction in polycystic ovary syndrome: from pathophysiological mechanisms to targeted therapies.Journal of ovarian research · 2026Review
- Polycystic ovarian syndrome a risk factor for non-communicable diseases: insights into recent research and prevention approaches.Journal of ovarian research · 2025Review
- ApoB100 and Atherosclerosis: What's New in the 21st Century?Metabolites · 2024Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
purposePolycystic ovary syndrome (PCOS) is a common reproductive endocrine disorder, which is closely associated with insulin resistance, glucose and lipid metabolism disorders. Patients with PCOS have a significantly higher risk of non-alcoholic fatty liver disease and are associated with hyperandrogenemia (HA). However, the exact mechanism by which HA exacerbates hepatic steatosis in PCOS has not yet been fully elucidated. This work aims to investigate the effects and underlying mechanisms of androgens on hepatic triglyceride (TG) metabolism in rats with PCOS.
methodsTwenty-four female Sprague-Dawley rats were randomly divided into four groups (6 rats/group): control, high-fat diet (HFD), PCOS, and PCOS + flutamide (Flu). Changes in the estrous cycle, liver and ovarian tissue sections, serum total testosterone, serum and liver biochemical indicators, and key enzymes involved in TG metabolism were studied.
resultsHepatocyte steatosis and TG accumulation were more evident in the PCOS group than in the control and HFD groups. The PCOS group showed apparent increases in the levels of serum alanine aminotransferase, aspartate aminotransferase, TG, free fatty acid, fasting insulin, and homeostasis model assessment of insulin resistance. Hepatic VLDL and apoB-100 levels decreased in the PCOS group. After Flu was administered to block the actions of androgens, the above abnormalities had been improved. The expression of MTTP was greatly decreased in the PCOS group and significantly increased after Flu administration.
conclusionHepatic steatosis in PCOS rats was correlated with HA. Androgens may exacerbate hepatic TG accumulation by downregulating MTTP expression in PCOS.
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Registered trials
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