MONDAY, Aug. 13 (HealthDay News) -- The bone hormone osteocalcin regulates beta-cell growth, insulin production and insulin sensitivity in mice, and protects them against obesity and diabetes, suggesting that the skeleton is an important regulator of glucose metabolism, according to a report in the Aug. 10 issue of Cell.
Gerard Karsenty, M.D., Ph.D., from Columbia University Medical Center in New York City, and colleagues generated mice lacking osteocalcin, which is secreted by osteoblasts. They had previously noted that these mice had an abnormal amount of visceral fat. They also produced mice whose osteoblasts lack the Esp gene, which increases osteocalcin.
The researchers found that the mice lacking osteocalcin had reduced proliferation of beta-cells as well as glucose intolerance and insulin resistance. The mice also had more fat, more adipocytes and higher serum triglyceride levels. Adding osteocalcin to beta-cells led to increased proliferation and insulin secretion, while adding osteocalcin to adipocytes led to increased production of adiponectin, a hormone that improves insulin sensitivity.
The investigators also found that mice lacking the Esp gene had increased proliferation of beta-cells and an increased production and sensitivity to insulin that protected them from induced obesity and diabetes.
"By revealing that the skeleton exerts an endocrine regulation of sugar homeostasis, this study expands the biological importance of this organ and our understanding of energy metabolism," Karsenty and colleagues conclude.
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