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A Hyperandrogenic Mouse Model to Study Polycystic Ovary Syndrome
Published on: October 2, 2018
Prenatal androgen exposure programs metabolic dysfunction in female mice.
Alison V Roland1, Craig S Nunemaker, Susanna R Keller
1Departments of Medicine Cell Biology, University of Virginia, PO Box 800578, Charlottesville, Virginia 22908, USA.
The Journal of Endocrinology
|August 18, 2010
Summary
Prenatal androgen exposure in female mice programs long-term metabolic dysfunction, including impaired glucose tolerance and altered adipocyte function, contributing to polycystic ovary syndrome (PCOS) development.
Area of Science:
- Endocrinology
- Reproductive Biology
- Metabolic Syndrome
Background:
- Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder affecting fertility and metabolic health.
- Previous studies established a prenatally androgenized (PNA) mouse model exhibiting reproductive abnormalities relevant to PCOS.
- The metabolic consequences of in utero androgen exposure in this PCOS model remained largely uncharacterized.
Purpose of the Study:
- To investigate the metabolic characteristics of female PNA mice, focusing on glucose homeostasis, insulin sensitivity, and adipocyte function.
- To determine if prenatal androgen exposure induces lasting metabolic alterations independent of age and body composition.
- To explore the direct effects of androgens on pancreatic islet function.
Main Methods:
- Assessment of fasting glucose, glucose tolerance tests, and body composition in female PNA mice and controls.
- Evaluation of peripheral insulin sensitivity.
- Analysis of pancreatic islet function through glucose stimulation assays, both in vivo and in vitro.
- Histological examination of visceral adipocytes.
Main Results:
- PNA mice displayed elevated fasting glucose and impaired glucose tolerance (IGT) irrespective of age.
- IGT was linked to pancreatic islet dysfunction and reduced insulin secretion, not peripheral insulin resistance or altered body composition.
- In vitro androgen exposure impaired isolated islet glucose response, suggesting direct activational effects.
- Visceral adipocytes were enlarged in PNA mice, indicating altered adipogenesis or function.
Conclusions:
- In utero androgen exposure induces significant and persistent metabolic disturbances in female mice, including impaired glucose metabolism and adipocyte alterations.
- These findings highlight a potential mechanism linking prenatal androgen excess to the metabolic sequelae observed in PCOS.
- Androgens may exert both organizational and activational effects on pancreatic islet function, contributing to metabolic dysfunction.
