Endocrine Abstracts

Polycystic ovarian syndrome (PCOS) is one of the commonest endocrine disorders of young women, and the commonest cause of reduced fertility in this age group. There are fundamental metabolic disturbances integral to the syndrome that lead to significant cardiovascular risk, and these include obesity, insulin resistance, beta cell dysfunction, impaired glucose tolerance and type 2 diabetes, dyslipidemia, hypertension, obstructive sleep apnoea, a pro-coagulant state, and endothelial dysfunction. All of these features are being seen with increasing frequency as the obesity epidemic extends into the paediatric age range. In some parts of the UK overweight and obesity affects up to 25% of the teenage population, and these young people demonstrate hyperinsulinism and tissue insulin resistance. The insulin resistance seen in PCOS is related to overweight and obesity; there is a hyperbolic relation between decreasing insulin sensitivity and increasing BMI. A new area of concern is the recognition of PCOS in teenage girls with type 1 diabetes: with increasing weight gain, they become insulin resistant, and are made hyperinsulinaemic with exogenous insulin, especially with aggressive insulin regimes. However obesity is not the only cause of insulin resistance in PCOS: insulin resistance is higher, and the glucose disposition index is lower, in women with PCOS and a family history of type 2 diabetes. In addition, insulin resistance also occurs in non-obese women with PCOS and normal glucose tolerance. Hyperinsulinism consistent with insulin resistance may precede and facilitate the androgen excess observed in PCOS. Insulin resistance is known to rise during puberty, resolving by Tanner stage 5. However in girls with premature adrenarche, this pubertal rise in insulin resistance is greatly exaggerated, and these girls appear to be at significantly higher risk for developing functional hyperandrogenism and PCOS.