Osteocalcin is inversely associated with glucose levels in middle‐aged Tibetan men with different degrees of glucose tolerance

Abstract Background Research on the characteristics and mechanisms of diabetes in Tibetans is scant. Especially, there is no study on the relationship between osteocalcin and glucose metabolism. The objective of this study was to investigate the associations of serum total osteocalcin (tOC) and undercarboxylated osteocalcin (ucOC) with glucose and lipid metabolism in Chinese indigenous Tibetans with different degrees of glucose tolerance. Methods In this study, 160 middle‐aged Tibetan men were involved, including 46 subjects with normal glucose tolerance (NGT), 52 subjects with impaired glucose regulation (IGR) and 62 subjects with type 2 diabetes. The homeostasis model assessment (HOMA) parameters, including HOMA‐IR and HOMA‐B, were used to estimate insulin resistance and β ‐cell function, respectively. Adiponectin, leptin, testosterone, 1,25‐dihydroxyvitamin D, tOC and ucOC were measured using ELISA kits. Results After adjustment for age and body mass index, plasma tOC level was correlated negatively with fasting and 30‐min post‐OGTT glucose, HOMA‐IR, leptin and testosterone; plasma ucOC level was correlated negatively with 30‐min post‐OGTT glucose, total cholesterol and 1,25‐dihydroxyvitamin D; ucOC : tOC was correlated positively with leptin. The negative association between HOMA‐IR and tOC remained significant after correcting for adiponectin; however, the association disappeared after correcting for leptin. HOMA‐IR was correlated negatively with age, adiponectin and tOC, and positively with total cholesterol, triglyceride and leptin. Stepwise linear regression analysis revealed that total cholesterol, leptin and adiponectin were independent predictors for HOMA‐IR in all subjects. Conclusions Our data support a link between osteocalcin and glucose metabolism in middle‐aged Tibetan men. The improved glucose tolerance exerted by tOC may be related to improved insulin sensitivity rather than improved β ‐cell function. Copyright © 2013 John Wiley & Sons, Ltd.