Endocrine Abstracts

Introduction: Recent animal’s studies suggest that osteocalcin have influence on beta cell proliferation, insulin secretion and insulin sensitivity. Osteoblasts appear to regulate energy expenditure by acting on adipocytes and pancreatic islet cells via osteocalcin, a 49-residue polypeptide. In turn, adipose tissue may also influence bone remodeling by regulating the activity of osteoblasts through adipokines, including leptin and adiponectin. Some of the complex mechanisms by which adipose tissue, brain and bone are able to regulate energy expenditure and glucose homeostasis are elucidated by recent studies.

Aim of the study: To investigate relationship between osteocalcin and insulin resistance in obese women with normal glucose tolerance.

Method: Fifty nine obese women (mean BMI=35.2±5.7 kg/m², mean age=36.4±10.2 years) participated in this study. We measured serum osteocalcin, fasting insulin level, fasting glucose level, HOMA-IR (Homeostasis model assessment of insulin resistance), AUC glucose (2 h OGTT), AUC insulin (2 h OGTT), adiponectin level and anthropometric parameters (body mass index, waist to hip ratio, total body fat). Statistics analysis was performed by SPSS 19. Pearson’s correlation coefficients were calculated to evaluate the relationship between osteocalcin and other parameters.

Results: Serum osteocalcin was inversely correlated with fasting plasma insulin (r=−0.379, P<0.05) and HOMA ir (r=−0.349, P<0.05) and positively correlated with adiponectin level (r=0.603, P<0.05). There was no statistically significant correlation between serum osteocalcin and fasting plasma glucose, AUC glucose, AUC insulin and anthropometric values (body mass index, waist to hip ratio, total body fat).

Conclusion: Our results confirmed significant correlation between insulin and insulin sensitivity with osteocalcin as well as with adiponectin, which suggests possible novel role of bone via osteocalcin in regulation of glucose metabolism and insulin sensitivity.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details unavailable.