Evolution of metabolic alterations 5 Years after early puberty in a cohort of girls predisposed to polycystic ovary syndrome.

Background: We and others have observed that young girls predisposed to polycystic ovary syndrome (PCOS) display defective insulin sensitivity, beta-cell function and non-esterified fatty acids (NEFA) suppressibility during early pubertal years, compared to controls. Our objective is to assess whether these differences in glucose and NEFA metabolisms persist after 5 years in late/post-puberty.

Methods: We conducted a prospective cohort study between 2007 and 2015 with 4-6 years of follow-up in an academic institution research center.

Adipose tissue insulin resistance in peripubertal girls with first-degree family history of polycystic ovary syndrome.

Objective: To assess metabolic and endocrine defects in girls genetically predisposed to polycystic ovary syndrome (PCOS).

Design: Controlled cross-sectional study.

Setting: University hospital.

Insulin and hyperandrogenism in women with polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is a very common endocrine disorder characterized by chronic anovulation, clinical and/or biochemical hyperandrogenism, and/or polycystic ovaries. But most experts consider that hyperandrogenism is the main characteristic of PCOS. Several theories propose different mechanisms to explain PCOS manifestations: (1) a primary enzymatic default in the ovarian and/or adrenal steroidogenesis; (2) an impairment in gonadotropin releasing hormone (GnRH) secretion that promotes luteal hormone (LH) secretion; or (3) alterations in insulin actions that lead to insulin resistance with compensatory hyperinsulinemia.