Polycystic ovary syndrome (PCOS), a condition associated with hyperandrogenemia, hyperinsulinemia and insulin resistance, is also presented with an increased risk for atherosclerosis. Advanced glycation end products (AGE) being a diverse and heterogeneous group of compounds have been implicated in the pathogenesis of many disorders including diabetic microvascular complications, connective tissue diseases particular in rheumatoid arthritis and neurologic conditions such as Alzheimer’s disease, as well as end-stage renal failure. Interestingly, it has been shown that precooked meals, overcooked food and several contemporary beverages contain increased amounts of AGEs which appeared to be absorbed by the intestinal tract. It is possible that this environmental contribution of exogenous AGEs to the endogenous pool in the general population and in particular in patients with increased endogenous AGE levels may be involved in the pathogenesis of atherogenesis or in the acceleration of its appearance. Recently, we have demonstrated increased AGE levels in women with PCOS which may be implicated in the endothelial dysfunction and infertility underlying this disorder.
The present chapter focuses on the detrimental effects of progressive AGE accumulation in the human body with particular emphasis on the pathological crosslinking of collagen formation, as well as on the endothelial dysfunction through increased oxidative stress, vasoconstriction, and creation of a procoangulant state and induction of pro-inflammatory responses. All these effects can alter the ovarian structure, its hormonal milieu and the whole reproductive function, further contributing to the infertility underlying the pathogenesis of PCOS.