Researchers led by Thomas Clemens of Johns Hopkins University School of Medicine engineered mice so that their osteoblasts or bone forming cells no longer displayed insulin receptors. These mice developed a bone-making deficiency, having thinner bones with fewer osteoblasts. Their results suggest that insulin is necessary for mice to maintain normal bone mass. Dr. Clemens pointed out that type 1 diabetics who do not have insulin frequently have low bone mass, suggesting that the results may be relevant for humans. The team also found that these mice gained weight as they aged- a phenomenon not related to eating. In time they developed resistance to insulin “ a condition seen in type 2 diabetics. The weight gain explains Clemens could be related to the bone hormone osteocalcin. The reason these mice are fat is because they're not making enough insulin, which is because they're not making osteocalcin, Clemens says. To confirm this, the researchers gave the insulin receptor-deficient mice osteocalcin, which improved their metabolic abnormalities.

In the second study led by Gerard Karsenty of Columbia University, insulin stimulates osteoblasts to produce an inactive form of osteocalcin that sticks to bone and doesn't enter circulation to stimulate the pancreas to secrete more osteocalcin. This inactive osteocalcin then erodes the bone with the help of osteoclasts. This explains the bone depletion process. Bone depletion or resorption the team found was linked to insulin secretion. The significance of this is that bone is an integrated part of how whole body glucose equilibrium is regulated. Drugs that inhibit bone resorption [which are commonly used to treat osteoporosis] may, in certain patients, favor glucose intolerance, Karsenty says. He adds that this is a concern that also needs to be addressed in future studies.