The Link Between Polycystic Ovary Syndrome and Both Type 1 and Type 2 Diabetes Mellitus

What Do We Know Today?

Thomas M Barber; Stephen Franks

Disclosures

Women's Health. 2012;8(2):147-154. 

In This Article

Future Perspective

The link between PCOS and T2D stems from the association of each condition with obesity and insulin resistance. T2D develops in the context of insulin resistance combined with β-cell dysfunction, insulin deficiency and hyperglycemia. By contrast, PCOS develops in the context of insulin resistance and compensatory hyperinsulinemia. Insulin has pleiotropic actions including co-gonadotrophic effects on tissues, such as the ovaries, that remain insulin sensitive, thus augmenting ovarian theca cell steroidogenesis. By contrast, the link between T1D and PCOS does not result from obesity and insulin resistance, but rather from adverse effects of hyperinsulinemia that in turn result from exogenous administration of insulin with supraphysiological concentrations within the systemic circulation.

An inherent problem associated with complex obesity-related conditions such as PCOS, is the disentanglement of factors pertaining to PCOS per se versus obesity-related factors. A challenge for future research in this field is to gain a clearer understanding of the nonobesity related factors that influence susceptibility to development of PCOS. Over the next 5–10 years we will see published studies from GWAS in PCOS that will provide new insights into the pathogenesis of this complex condition. It is likely that hitherto unexpected genome sequences will be identified as susceptibility variants for PCOS. This will provide an opportunity for the development of genetic screening for the condition, and also enable future developments of novel therapeutic strategies for women with PCOS. As the obesity epidemic grows, obesity-related conditions such as PCOS and T2D will assume greater prominence. It is important to maintain close collaboration between the fields of obesity and the obesity-related conditions, to complement our understanding of pathogenesis, to broaden opportunities for future research and, ultimately, improve patient care.

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