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Your Bones May Regulate Your Metabolism and Weight

Can Building Bone Mass Help Control Insulin Resistance?

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Updated August 17, 2007

New research about the bones role in endocrine functions provides exciting insight into the ever expanding area of diabetes management. Scientists at Columbia University Medical Center have discovered that our bones do more than provide structural support our bodies. They also produce hormones that seem to regulate blood glucose and other functions of metabolism. This means that the skeleton may play more of a part in the functioning of the endocrine system than previously thought.

A press release from the university outlines the research that appeared in the August 10, 2007 edition of the journal, Cell. In a previous study, it was proven that the hormone leptin, a product of fat cells, controls bone mass. The scientists wondered if the process worked both ways. Does bone also communicate with fat cells? In order to answer this question, they looked for bone-forming cells that might talk to fat cells. They found osteocalcin, a hormone that does seem to have a relationship with fat cells but also does much more in the way of regulating metabolism and insulin receptivity. Osteocalcin appears to control blood glucose and fat deposits, and increases not only insulin sensitivity but also seems to raise insulin production in the pancreas. No other substance in the body appears to accomplish both tasks.

Gerald Karsenty, MD, PhD, and chair of the Genetics and Development department at Columbia University Medical Center in New York, states in the press release,

"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. These results uncover an important aspect of endocrinology that was unappreciated until now."

In the study, mice with high levels of osteocalcin did not gain weight and did not develop type 2 diabetes even when they ate a high fat diet. If the mice had low levels of the hormone, they did become obese, and did develop diabetes. People with type 2 diabetes have been shown to have low osteocalcin levels, also.

What are the implications of decreased osteocalcin levels and it's effects on metabolic syndrome and type 2 diabetes in people? It is true that exercise plays an important part in lowering blood glucose levels. It is also true that a sedentary lifestyle is partly responsible for the rise in the incidence of metabolic syndrome, insulin resistance and type 2 diabetes. Would it be possible that buidling bone mass through exercise would increase osteocalcin levels and in turn boost insulin production and receptivity?

Through email, I asked Dr. Karetsky his opinion. When asked if increasing bone mass through exercise and weight training would reduce the risk of metabolic syndrome. He replied that increasing bone mass should reduce the risk. He felt that increasing bone mass by exercise could increase osteocalcin secretion.

Type 2 diabetes and metabolic syndrome occur when metabolic functions like insulin production and insulin resistance get out of whack. Both conditions have been proven to be directly related to excess weight and a sedentary lifestyle. Increasing exercise and decreasing fat improves insulin production and decreases insulin resistance. And now it seems that there is new evidence that another way that is achieved is by hormones secreted by the bones.

Based on this study, it sounds like there may be one more good reason to exercise everyday. Exercise, especially working with weights, does build bone mass, which in turn increases the amount of osteocalcin that bones produce. The more osteocalcin, the better our insulin regulation and the better we can control our blood glucose levels.

Sources:

Streich, Elizabeth. "Press Release - Do Bones Help Control Metabolism and Weight?." Columbia University Medical Center. 09 Aug 2007. Columia University. 16 Aug 2007.

Na Kyung Lee, Hideaki Sowa, Eiichi Hinoi, Mathieu Ferron, Jong Deok Ahn, Cyrille Confavreux, Romain Dacquin, Patrick J. Mee, Marc D. McKee, Dae Young Jung, Zhiyou Zhang, Jason K. Kim, Franck Mauvais-Jarvis, Patricia Ducy, and Gerard Karsenty, "Endocrine Regulation of Energy Metabolism by the Skeleton." Cell 130(2007): 456-469.

"What is Exercise?" American Diabetes Association. ADA. 16 Aug 2007.[

Gerard Karsenty MD. Email response from Dr. Karsenty. 14 Aug 2007.

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