Contrary to the popular view of the skeleton as an inert, lifeless structure, it turns out that the bones play a number of roles in the body. According two animal studies recently published in the journal Cell, one of these roles is blood glucose regulation, suggesting that the skeleton may play a part in the development of Type 2 diabetes in some people.
Bone remodeling, a natural process in which bones are continually broken down and rebuilt, relies on the action of hormones such as parathyroid. Although bones cells have long been known to have insulin receptors on their surface, the effect(s) of insulin on bone has not been clear.
To investigate this relationship, two research teams worked with mice whose osteoblasts, or bone-making cells, were engineered not to have insulin receptors. The first team, from Johns Hopkins University School of Medicine, in Baltimore, found that the mice developed a bone-making deficiency, suggesting that insulin is integral to having normal bone mass. Moreover, this team discovered that as the mice aged, they became overweight and developed insulin resistance, even though they were eating the same amount as mice in a control group. The researchers were able to link this effect to a bone hormone called osteocalcin, which stimulates the pancreas to make insulin and sensitizes the body’s cells to its effects.
Lead author Thomas Clemens, PhD, says, “The reason these mice are fat is because they’re not making enough insulin, which is because they’re not making osteocalcin.”
The second research team, from Columbia University Medical Center, in New York City, found that insulin stimulates the creation of an inactive form of osteocalcin, which sets the bone-destroying osteoclast cells into motion, resulting in the breakdown of bone. This breakdown creates an environment that activates the osteocalcin, which then stimulates the production of more insulin.
“The significance of this is that bone is an integrated part of how whole body glucose equilibrium is regulated… This research has important implications for both diabetes and osteoporosis patients,” says lead study author Gerard Karsenty, MD, PhD. “First, [it] shows that osteocalcin is involved in diabetes onset. Secondly, bone may become a new target in the treatment of Type 2 diabetes, as it appears to contribute strongly to glucose intolerance. And finally, osteocalcin could become a treatment for Type 2 diabetes.”
Although in its early stages, this research may pave the way for novel treatments for Type 2 diabetes that use osteocalcin or otherwise focus on bone, according to the researchers.
For more information, read “Skeleton Key: Bone Cells May Play a Part in Regulating the Body’s Metabolism” or see the study summaries in Cell.
