As in any other endocrine pathway, it can be postulated that adipocytes and leptin production in turn , may be under a feedback regulatory control of bone metabolism. Osteocalcin, an osteoblast specific protein, seems a suitable candidate. Indeed, glucose intolerance and greater amounts of visceral fat were noted in Osteocalcin knockout mice
Furthermore, deletion of other genes in osteoblasts in mice led to pancreatic beta cell proliferaation, a rise in insulin secretion and sensitivity that protected against obesity and diabetes, demonstrating at last the capacity of osteoblasts tto contribute to energy metabolism.