The research demonstrates that bone cells release a hormone called osteocalcin, which controls the regulation of glucose and fat deposition through synergistic mechanisms previously not recognized. Usually, an increase in insulin secretion is accompanied by a decrease in insulin sensitivity. Osteocalcin, however, increases both the secretion and sensitivity of insulin, in addition to boosting the number of insulin-producing cells and reducing stores of fat. Osteocalcin produced by cells in bone interacts with beta cells in the pancreas and fat cells to improve the body's ability to handle sugar and keep fat mass low.
The authors showed that an increase in osteocalcin activity prevents the development of type 2 diabetes and obesity in mice. This discovery potentially opens the door for novel therapeutic avenues for the prevention and treatment of type 2 diabetes. “The discovery that our bones are responsible for regulating blood sugar in ways that were not known before completely changes our understanding of the function of the skeleton and uncovers a crucial aspect of energy metabolism,” said Gerard Karsenty, M.D., Ph.D., chair of the department of Genetics and Development at Columbia University Medical Center.
The researchers found that osteocalcin, a protein made only by osteoblasts, was not a mere structural protein, but rather a hormone with totally unanticipated and crucial functions. Osteocalcin directs the pancreas’ beta cells, which produce the body’s supply of insulin, to produce more insulin. At the same time, osteocalcin directs fat cells to release a hormone called adiponectin, which improves insulin sensitivity. This discovery showed for the first time that one hormone has a synergistic function in regulating insulin secretion and insulin sensitivity, and that this coordinating signal comes from the skeleton.
MEDICA.de; Source: Columbia University