Assessment of the Relationship between Serum Vitamin D and Osteocalcin Levels with Metabolic Syndrome in Non-Osteoporotic Postmenopausal Women.

Abstract

Introduction The aim of this study was to compare serum vitamin D and osteocalcin levels in non-osteoporotic postmenopausal women with and without metabolic syndrome and to analyze the relationship between serum vitamin D and osteocalcin levels and the relationships between these two factors and other clinical/biochemical parameters. Material and Method This cross-sectional study was carried out in 191 postmenopausal non-osteoporotic (T-score > − 2.5) women. Patients were divided into two groups according to the presence or absence of metabolic syndrome. Blood samples were obtained and evaluated for 25-hydroxyvitamin D, osteocalcin, insulin resistance (using a homeostatic model assessment of insulin resistance), glycosylated hemoglobin (HbA 1c ), calcium, phosphorus, deoxypyridinoline, thyroid-stimulating hormone, lipid profile, fasting insulin, fasting glucose and HbA 1c levels. Demographic and laboratory parameters were recorded for each woman. Results Vitamin D was found to be lower in women with metabolic syndrome compared to controls (16.1 ± 11.2 vs. 20.4 ± 13.1 mg/dL; p = 0.013). Similarly, osteocalcin was found to be significantly lower in the metabolic syndrome group compared to the control group (4.2 ± 2.1 vs. 5.5 ± 3.0; p < 0.001). A significant positive correlation was observed between vitamin D and osteocalcin levels (r = 0.198; p = 0.008). There was an inverse correlation between vitamin D and some of the lipid parameters. However, osteocalcin levels were negatively correlated with C-reactive protein, insulin resistance, and HbA 1c in both groups (p = 0.003, p = 0.001 and p = 0.048, respectively). Conclusion Vitamin D deficiency is common in postmenopausal women, even in women who are non-osteoporotic. Serum levels of vitamin D are significantly decreased in cases with metabolic syndrome. Vitamin D may directly improve serum lipid profiles and may indirectly decrease insulin resistance and subclinical systemic inflammation through the impact on the metabolic functions of osteocalcin.