Weight loss-induced increases in osteocalcin are associated with improvements in glucose homeostasisPamela S. Hinton1*, John P. Thyfault1, Tom R. Thomas1, Bryan K. Smith2, Joseph E. Donnelly2 and R. Scott Rector3
- corresponding Author:
- Pamela S. Hinton
Department of Nutrition and Exercise Physiology
University of Missouri-Columbia
106 McKee, Columbia, MO 65211
Tel: (573) 882-4137
FAX: (573) 884-4885
E-mail: [email protected]
Received Date: October 21, 2011; Accepted Date: November 22, 2011; Published Date: November 25, 2011
Citation: Hinton PS, Thyfault JP, Thomas TR, Smith BK, Donnelly JE, et al. (2011) Weight loss-induced increases in osteocalcin are associated with improvements in glucose homeostasis. Endocrinol Metabol Syndrome S1:002. doi: 10.4172/2161-1017.S1-002
Copyright: © 2011 Hinton PS, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: Recent data suggest that the weight loss-associated increase in the osteoblast-specific peptide osteocalcin (OC) might be related, not to increased bone formation, but to the endocrine action of OC enhance to both pancreatic insulin secretion and insulin sensitivity of target tissues. Thus, the purpose of the present study was to examine the possible role of serum OC as a regulator of glucose homeostasis following weight loss in sedentary overweight or obese women.
Methods: This study was a post hoc analysis of three independent weight-loss intervention studies, which varied in weight-loss magnitude and duration. Serum glucose, insulin, bone formation (OC and bone-specific alkaline phosphatase, BAP) and resorption (C-terminal peptide of type I collagen, CTX) markers were measured before and after weight loss in sedentary overweight or obese women (n=77) and were compared with data from active, lean controls (n=46).
Results: Fasting insulin, glucose and HOMA-IR significantly improved with weight loss. OC and CTX increased significantly following weight reduction, while BAP remained unchanged. The percent increase in OC was positively associated with the magnitude of the weight loss (r=0.25, p=0.02), while the increase in CTX was not (r=0.10, p=0.26). Following weight loss, serum OC was negatively associated with fasting glucose (r= -0.232, p=0.02), and weight-lossassociated changes in serum OC were positively correlated with changes in HOMA2-%B (r=0.33, p=0.04).
Conclusions: These preliminary results suggest that OC might play a role in the improvements in glucoregulation observed following weight reduction in overweight, sedentary women.