Introduction

The interaction between excess adiposity and disturbed female fertility is best represented by polycystic ovary syndrome (PCOS). This syndrome has been studied by both gynaecologists and endocrinologists as the mechanisms leading to its diverse manifestations are complex. PCOS is very common in the developed world, with up to 10% of premenopausal women being affected. Clinically, PCOS is characterised by the development of hirsutism, oligo-ovulation/anovulation and subfertility/infertility. The pathophysiology of the syndrome, even though not yet fully delineated, implicates insulin resistance as a central factor as it leads to hyperinsulinaemia and androgen excess. High circulating insulin levels inhibit the production of sex hormone-binding globulin (SHBG) from the liver and directly cause excess androgen production at the level of the ovary. These two processes lead to the aesthetically troublesome hirsutism and contribute to irregular menses or even cause secondary amenorrhoea. However, it is even more worrying that women with PCOS are at increased risk of cardiovascular mortality and morbidity owing to their occult disturbed metabolism, which shares features of the metabolic syndrome. These include impaired glucose tolerance and type 2 diabetes, hypertension, dyslipidaemia and increased waist circumference.

Approximately 40% of women living in the developed world are obese or overweight. The prevalence of obesity in women with PCOS varies widely, from 10% to 70% of cases. Modest weight loss can, however, reverse many of the features of the syndrome and lower the cardiometabolic risk profile.

This review focuses on the treatment of obesity in the context of PCOS with antiobesity medication and obesity (bariatric) surgery. Metformin and rimonabant are not reviewed here as the former is an insulin sensitiser and its effects on weight reduction in women with PCOS have been discouraging and the latter has been withdrawn from the market.