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A Hyperandrogenic Mouse Model to Study Polycystic Ovary Syndrome
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Prenatal hyperandrogenism induces alterations that affect liver lipid metabolism

Giselle Adriana Abruzzese1, Maria Florencia Heber2, Silvana Rocio Ferreira2

  • 1Laboratorio de Fisio-patología OváricaCentro de Estudios Farmacológicos y Botánicos (CEFYBO), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Facultad de Medicina, Universidad de Buenos Aires (UBA), Buenos Aires, Argentina giselleabruzzese@gmail.com.

The Journal of Endocrinology
|May 15, 2016
PubMed

Insights

Prenatal androgen exposure in rats leads to polycystic ovary syndrome (PCOS)-like conditions with altered liver lipid metabolism and increased metabolic syndrome risk. Anovulatory PCOS phenotypes showed greater susceptibility to fatty liver development.

Area of Science:

  • Endocrinology
  • Hepatology
  • Reproductive Biology

Background:

  • Polycystic ovary syndrome (PCOS) is linked to increased risk of fatty liver and steatosis.
  • Prenatal hyperandrogenism is a proposed contributing factor to PCOS development.

Purpose of the Study:

  • To investigate the impact of prenatal hyperandrogenism on liver lipid metabolism and fatty liver development in a rat model.
  • To assess the metabolic consequences and liver alterations in prenatally hyperandrogenized offspring mimicking PCOS phenotypes.

Main Methods:

  • Pregnant rats were administered testosterone to induce prenatal hyperandrogenism.
  • Offspring were evaluated at pubertal age for ovulatory/anovulatory phenotypes, liver parameters, and metabolic status.
  • Key assessments included hepatic enzymes, lipid content, lipogenesis/fatty acid oxidation, oxidant/antioxidant balance, inflammation markers, glucose metabolism, and lipid profiles.

Main Results:

  • Prenatally hyperandrogenized (PH) offspring, regardless of ovulatory status, exhibited altered lipogenesis and fatty acid oxidation pathways.
  • PH groups showed impaired oxidant/antioxidant balance, reduced inflammation markers, decreased glucose tolerance, and dyslipidemia.
  • Neither PH group displayed overt fatty liver, but the anovulatory phenotype (PHanov) showed more pronounced alterations in liver lipogenesis and glucose/insulin metabolism, indicating higher steatosis susceptibility.

Conclusions:

  • Prenatal hyperandrogenism induces PCOS-like phenotypes in female offspring with significant liver alterations and metabolic syndrome risk.
  • The study highlights altered lipid metabolism and oxidative stress as key factors in the development of PCOS-related complications.
  • The anovulatory PCOS phenotype is more vulnerable to hepatic steatosis due to exacerbated metabolic and lipogenic dysregulation.

Keywords:
fatty liverlipid metabolismpolycystic ovary syndromeprenatal hyperandrogenism

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