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Intriguing studies suggest that osteocalcin (OC) and its carboxylated (Gla)/uncarboxylated form are involved in the regulation of insulin secretion and action. Additionally, advanced glycated end products (AGEs) directly regulate the secretion of these osteoblast-derived molecules. In polycystic ovarian syndrome (PCOS), among the pathophysiological aberrations, deregulation of insulin secretion and action as well as elevated AGEs levels have been demonstrated. In this study, we evaluated the serum levels of osteocalcin and Gla osteocalcin and their possible associations with metabolic, hormonal, and ultrasonographic components of PSOS: 97 women were studied, 50 PCOS patients and 47 controls, matched for age and body mass index (BMI). In each subject, the levels of bone metabolism markers have been evaluated, and metabolic and hormonal profiles as well as ovarian ultrasound were carried out. Osteocalcin (4.30 ± 1.74 vs. 6.20 ± 1.78 ng/ml, P < 0.0005) values were significantly lower, whereas Gla osteocalcin (37.93 ± 6.87 vs. 9.64 ± 8.21 ng/ml, P < 0.0005) and receptor activator for nuclear factor-κB ligand (0.54 ± 0.26 vs. 0.16 ± 0.15 pmol/l, P < 0.0005) values were significantly higher in PCOS subjects compared to the control group, independently of obesity. A significant association was disclosed between osteocalcin and Gla osteocalcin with androgens, insulin resistance, AGEs, and ovarian morphology. Receiver operating curve analysis revealed that Gla osteocalcin [AUC, 0.975 (95% CI, 0.93–1.00)] as well as AGEs are significant prognostic factors of PCOS [AUC, 0.986 (95% CI, 0.97–1.00)]. Lower osteocalcin and elevated serum levels of its carboxylated form are displayed in PCOS subjects and are associated with several PCOS components. These findings suggest a potential interaction between bone-derived markers and the metabolic/hormonal abnormalities observed in PCOS. However, the pathophysiological mechanisms and moreover the possible clinical implications require further investigation.

ObjectiveOocyte maturation process characterizes polycystic ovary syndrome (PCOS). The mechanisms of this abnormality leading to chronic anovulation are under investigation. Advanced glycosylated end products (AGEs), a marker of oxidative stress linked with oocyte maturation are localized in granulosa cells and are increased in sera, in women with PCOS. The aim of this study was to investigate the relationship, whether there is an association between the anti-mullerian hormone (AMH), a hormone produced by granulosa cells and AGEs in ovulatory and anovulatory PCOS (PCOS-Anov), as well as in non-PCOS anovulatory (Non-PCOS Anov) women.DesignCross-sectional study.MethodsData from sixty women with PCOS (37 anovulatory and 23 regularly ovulating) were compared with eleven Non-PCOS Anov women and 25 normal women. In each subject biochemical, hormonal, and ultrasonographic parameters were studied.ResultsAMH values were statistically significantly higher in PCOS-Anov (7.63±3.12) in comparison with ovulatory PCOS (PCOS-Ov; 4.92±2.50), Non-PCOS Anov (3.66±1.4), and controls (4.02±1.27 ng/ml). AGEs demonstrated a similar pattern: 8.70±1.65 in PCOS-Anov, 7.43±1.79, PCOS-Ov, 5.21±0.09, Non-PCOS Anov, and 5.85±0.89 U/ml in controls (Pr: 0.326,Pr: 0.42,P: 0.0001) and the presence of anovulation.ConclusionsThese data suggest that an oxidative marker, AGEs, and AMH, may interact in the anovulatory mechanisms in women with PCOS.

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.