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article imageOur Skelton Helps Control Sugar Metabolism

By Bob Ewing     Aug 11, 2007 in Science
A recent study has shown that our bones are more than just the remains of our bodies. Our bones play a role in sugar metabolism and weight. Bone cells release a hormone called osteocalcin,
When and if we think of our bones we usually call up the well-known skeleton. The skeleton is a familiar Halloween figure that until recently was considered to be nothing more than a calcified inert structure.
Researchers, working out of the Columbia University Medical centre, have shed a new light on those old bones. The team demonstrated that the skeleton is in fact an endocrine organ and that this organ helps control our metabolism and our weight. This means that our skeleton is a determinant of the development of type 2 diabetes.
The study was published in the August 10 issue of Cell and shows that the bone cells release a hormone that is called osteocalcin. Osteocalcin controls the regulation of blood sugar (glucose) and fat deposition through synergistic mechanisms previously that had not been previously recognized.
An increase in insulin secretion is, normally, accompanied by a decrease in insulin sensitivity.
The role that osteocalcin plays is to increase both the secretion and sensitivity of insulin, and it also boosts the number of insulin-producing cells and reducing stores of fat.
According to the study, an increase in osteocalcin activity prevents the development of type 2 diabetes and obesity in mice. This find means that there are possibilities for the development of 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 Karentsy M.D. PhD
The team already were aware that leptin, a hormone released by fat cells, acts upon and ultimately controls bone mass. This led them to reason that bones must in turn communicate with fat, so they searched bone-forming cells for molecules that could potentially send signals back to fat cells.
The outcome of their inquiry was the finding that osteocalcin, which is a protein made only by bone-forming cells (osteoblasts), was not simply a structural protein, but was a hormone that possessed unanticipated and crucial functions.
The study showed that osteocalcin directs the pancreas’ beta cells, which produce the body’s supply of insulin, to produce more insulin and that osteocalcin also directs fat cells to release a hormone called adiponectin, which improves insulin sensitivity.
This was the first time that a study had discovered that one hormone has a synergistic function in regulating insulin secretion and insulin sensitivity, and that this coordinating signal comes from the skeleton.
Another function that osteocalcin performs is to enhance the production of insulin-producing beta cells. The production of insulin producing beta cells is considered to be one of the best, currently unattainable, strategies to treat diabetes.
It has been previously show that people with type 2 diabetes have low osteocalcin levels, suggesting so that altering the activity of this molecule could be an effective therapy.
Prior research at Columbia has shown that mice with high levels of osteocalcin activity were prevented from gaining weight or becoming diabetic even when they ate a high fat diet. When the mice without osteocalcin protein were analyzed it was shown that they had type 2 diabetes, increased fat mass, a decrease in insulin and adiponectin expression, and decreased beta-cell proliferation.
Currently the research team is investigating the role of osteocalcin in the regulation of blood sugar in humans as well as continuing investigations into the relationship between osteocalcin and the appearance of type 2 diabetes and obesity
More about Bone, Therapeutic target, For type diabetes
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