The exact cause of PCOS is unknown but is likely to be due to a combination of both genetic factors and environmental factors. The genetic factors proposed to potentially contribute to PCOS include abnormalities in gonadotrophin action and steroidogenesis. There is also proposed to be inherent abnormalities in the action of insulin leading to insulin resistance and consequent elevated circulating insulin levels or hyperinsulinaemia.

Insulin resistance is defined as the reduced ability of insulin to exert its physiological effect at normal concentrations and is manifested peripherally at the tissues or centrally at the liver. In PCOS, the exact mechanism for insulin resistance is not yet known, although there may be an abnormal constitutive serine phosphorylation of the insulin receptor in a proportion of women. A significant majority of women with PCOS (up to 70 per cent) are more insulin resistant than controls matched for body-mass index, fat free body mass, and body-fat distribution^3,4.

Insulin resistance and hyperinsulinaemia contribute to the reproductive hormonal features of PCOS through insulin stimulating ovarian androgen production and decreasing sex hormone-binding globulin (SHBG) production at the liver. This leads to increased concentrations of total and free androgens with consequent effects on tissues such as the skin (leading to hirsutism and acne) and the ovaries (leading to lack of ovulation, menstrual irregularity and infertility). Although not all women with PCOS are insulin resistant, women with PCOS who are insulin resistant have worsened reproductive and metabolic abnormalities than insulin sensitive women with PCOS.

Weight gain and abdominal weight gain also lead to insulin resistance and hyperinsulinaemia. This is likely to be through different mechanisms to the specific insulin resistance present in PCOS. This means that when a woman with PCOS gains weight, this will further worsen her insulin resistance and her reproductive and metabolic symptoms. For example, rates of IGT and DM2 are elevated in lean compared to obese women with PCOS (10.3 per cent and 1.5 per cent compared to 31.3 per cent and 7.5 per cent respectively)⁵. In 394 women with PCOS, women in the upper BMI quartile were 13.7 times more likely to have the metabolic syndrome compared to those in the lowest quartile⁶. Women with PCOS tend to have a body mass index (BMI) outside the acceptable range (19-25 kg/m2) with 40-60 per cent reported as overweight or obese⁷. In a recent study, women with PCOS (n=401) demonstrated a lower proportion of BMI < 25 kg/m2 and higher proportion of BMI > 30 kg/m2 and 40 kg/m2 compared to age-matched non-PCOS controls (n=2586)⁸. Women with PCOS also display an increased central or visceral distribution of adiposity⁹. This is observed even in lean women with PCOS compared to weight-matched controls^10,11. Where the presentation of PCOS is worsened by IR and being an unhealthy weight, these represent important intervention targets in the community.

Content updated 20 November, 2009