Androgens and polycystic ovary syndrome

Figures & data

Figure 1. Unifying hypothesis explaining the interplay between the polycystic ovary syndrome and abdominal adiposity.

This interplay is the result of a vicious circle represented by the solid arrows: androgen excess favors the abdominal deposition of body fat, and visceral fat facilitates androgen excess of ovarian and/or adrenal origin by the direct effects (dashed arrow) of several autocrine, paracrine and endocrine mediators, or indirectly by the induction of insulin resistance and hyperinsulinism.

Reproduced from [6], with permission. © Elsevier (2007).

Figure 2. Polycystic ovary syndrome as the result of the interaction of a primary abnormality in androgen synthesis, manifesting as androgen excess, with environmental factors such as abdominal adiposity, obesity and insulin resistance.

In one extreme (†), in some patients, the disorder is severe enough to result in polycystic ovary syndrome even in the absence of triggering environmental factors. In the other extreme (‡), a very mild defect in androgen secretion is amplified by the coexistence of abdominal adiposity, obesity and/or insulin resistance. Between the two extremes, there is a spectrum in the severity of the primary defect in androgen secretion, explaining the heterogeneity of polycystic ovary syndrome patients with regards to the presence of obesity and metabolic comorbidities. However, patients share a primary defect in androgen secretion.

Reproduced from [6], with permission. © Elsevier (2007).

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Escobar-Morreale HF, San Millan JL. Abdominal adiposity and the polycystic ovary syndrome. Trends Endocrinol. Metab.18, 266–272 (2007).

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