Introduction

The first reports of a link between insulin and polycystic ovary syndrome (PCOS) appeared in the 1980s. First there was the demonstration of a link between hyperinsulinism and hyperandrogenism and then, soon after, the demonstration that non-obese women with PCOS were insulin resistant. These two seminal papers opened up a whole new field of investigation exploring the relationship between what was later to be called the metabolic syndrome and PCOS.

Much of the initial work in this area focused on the correlation between insulin and androgens in the circulation, with a debate surrounding the direction of causation in this relationship. A consensus view gradually emerged supporting the role of insulin as a co-gonadotrophin amplifying the effect of luteinising hormone (LH) on theca cell testosterone production. Recently, the opposing view that androgens might induce a state of insulin resistance has gained attention again.

Recognition that insulin has a pathogenic role in PCOS has led to several new treatment strategies and branches of research:

1. ∎ Addressing insulin resistance by any means has become routine in the management of PCOS.

2. ∎ Elements of the insulin-signalling pathway have been explored as candidates for the inheritance of PCOS.

3. ∎ The importance of PCOS in identifying individuals and family members at risk of developing type 2 diabetes has become an important part of preventive medicine.

Definitions and diagnosis

In clinical practice, the diagnosis of PCOS is relatively straightforward according to European guidelines. A more contentious area is the assessment of the metabolic syndrome in PCOS. Most clinical guidelines agree that an assessment of insulin status in individuals suspected of having the metabolic syndrome is not required in routine practice. If one is concerned, however, not to miss an opportunity to prevent transition to type 2 diabetes later in life, then metabolic status has to be addressed.