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Research shows skeleton to be endocrine organ

g cells for molecules that could potentially send signals back to fat cells.

The researchers found that osteocalcin, a protein made only by bone-forming cells (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 bodys 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. Additionally, osteocalcin enhances the production of insulin-producing beta cells, which is considered one of the best, but currently unattainable, strategies to treat diabetes.

People with type 2 diabetes have been shown to have low osteocalcin levels, suggesting that altering the activity of this molecule could be an effective therapy. That hypothesis is supported by the Columbia research, which showed that mice with high levels of osteocalcin activity were prevented from gaining weight or becoming diabetic even when they ate a high fat diet. Analysis of mice lacking the osteocalcin protein showed that they had type 2 diabetes, increased fat mass, a decrease in insulin and adiponectin expression, and decreased beta-cell proliferation.

This research was supported by the National Institutes of Health, the American Diabetes Association, the Japan Society for the Promotion of Science, and the Pennsylvania Department of Health.

The researchers are now examining the role of osteocalcin in the regulation of blood sugar in humans and are continuing investigations into the relationship between osteocalcin and the appearance of type 2 diabetes and obesity.


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Contact: Susan Craig
sc2756@columbia.edu
212-305-9746
Columbia University Medical Center
9-Aug-2007


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