ECE2010 Poster Presentations Female reproduction (44 abstracts)
1Endocrine Section, First Department of Medicine, University of Athens Medical School, Athens, Greece; 2Division of Endocrinology and Human Reproduction, Second Department of Obstetrics and Gynecology, Aristotle University of Thessaloniki, Thessaloniki, Greece; 3Laboratory of Biological Chemistry, University of Athens Medical School, Athens, Greece.
Objective: 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 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 OC and Gla and their possible associations with PCOS metabolic, hormonal and ultrasonographic components.
Research design and methods: Of 97 women were studied, 50 PCOS and 47 controls, age and BMI-matched. In each subject the levels of bone metabolism markers have been evaluated and metabolic, hormonal profiles as well as ovarian ultrasound were carried out.
Results: Osteocalcin (4.30±1.74 vs 6.20±1.78 ng/ml, P<0.0005) values were significantly lower, whereas Gla (37.93±6.87 vs 9.64±8.21 ng/ml, P<0.0005) and RANKL (0.54±0.26 vs 0.16±0.15 pmol/l, P<0.0005) values were significantly higher, in PCOS subjects compared to control group, independently of obesity. A significant association was disclosed between osteocalcin and Gla with androgens, insulin resistance, AGEs and ovarian morphology. ROC analysis revealed that Gla (AUC 0.975 (95% CI 0.931.00)), as well as AGEs are significant prognostic factor of PCOS existence (AUC 0.986 (95% CI 0.971.00)).
Conclusions: 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 metabolic/hormonal abnormalities observed in PCOS. However, the pathophysiological mechanisms and more over the possible clinical implications require further investigation.