Androgen excess and metabolic disorders in women with PCOS: beyond the body mass index
Insulin resistance is a common feature among women with polycystic ovary syndrome (PCOS), especially in those patients with hyperandrogenism and chronic anovulation. PCOS women are at risk for developing metabolic syndrome, impaired glucose tolerance and type II diabetes mellitus (DM II).
The aim of this review is to explore the existing knowledge of the interplay between androgen excess, pancreatic β-cell function, non-alcoholic fatty liver disease (NAFLD), intra-abdominal and subcutaneous (SC) abdominal adipocytes in PCOS, providing a better comprehension of the molecular mechanisms of diabetologic interest.
A comprehensive MEDLINE® search was performed using relevant key terms for PCOS and DM II.
Insulin-induced hyperandrogenism could impair pancreatic β-cell function, the SC abdominal adipocytes’ lipid storage capacity, leading to intra-abdominal adipocyte hypertrophy and lipotoxicity, which in turn promotes insulin resistance, and could enhance NAFLD. Fetal hyperandrogenism exposure prompts to metabolic disorders. Treatment with flutamide showed to partially reverse insulin resistance.
Metabolic impairment seems not to be dependent only on the total fat mass content and body weight in women with PCOS and might be ascribed to the androgen excess.
KeywordsPCOS Insulin resistance Obesity Hyperandrogenism
American Association of Clinical Endocrinology
American College of Endocrinology
Body mass index
- DM II
Type II diabetes mellitus
De novo methyl-transferase 3
Free fatty acids
First phase insulin response
Impaired glucose tolerance
Non-alcoholic fatty liver disease
National Institutes of Health
Oral glucose tolerance test
Polycystic ovary syndrome
Sex hormone-binding globulin
Steady-state plasma glucose
Compliance with ethical standards
Conflict of interest
The authors declare that there is no conflict of interest regarding the publication of this paper.
This article does not contain studies with human participants or animals performed by any of the authors.
No informed consent.
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