Obesity and polycystic ovary syndrome: pathophysiological link and impact on patients’ phenotype

Abstract

Polycystic ovary syndrome (PCOS) is a complex and common endocrine disorder affecting reproductive-aged women. The etiology of polycystic ovary syndrome remains unclear but increasing evidence supports a central role of insulin resistance and its compensatory hyperinsulinemia in the pathogenesis of the syndrome. Insulin resistance is inherent to PCOS, however, it can be exacerbated by overweight, obesity and especially by central obesity, with possible consequences on the syndrome phenotype. The exact prevalence of obesity in women with polycystic ovary syndrome is not known, however, higher global adiposity and increased amounts of visceral adipose tissue are commonly observed in these patients seeming to vary with age, race, genetic and environmental factors. Although some studies suggest that obesity has little impact on symptoms, features or development of polycystic ovary syndrome, many data report that excess body weight and visceral fat accumulation may worsen certain aspects of the phenotype including biochemical hyperandrogenemia, menstrual disorders, chronic anovulation and some metabolic abnormalities such as dyslipidemia, glucose intolerance and hypertension, raising the risk for infertility, diabetes mellitus, atherosclerosis, clinical and subclinical cardiovascular disease. Obesity in women with polycystic ovary syndrome has also been associated with a poor response to infertility treatment, high risk for pregnancy complications, elevated risk for endometrial cancer and increased psychological comorbidities. Therefore, weight loss with lifestyle therapy, pharmacological treatment and bariatric surgery is considered the first-line therapy in obese women with polycystic ovary syndrome. Weight loss improves insulin resistance and hyperandrogenism with benefits in many features, especially metabolic and reproductive abnormalities.