A new study led by Mathieu Ferron from the Montreal Clinical Research Institute (IRCM), address the effect of a hormone called osteocalcin, produced by the bones, on appetite and metabolism of sugars and fat. The study was published in The Journal of Clinical Investigation.

Bone: An endocrine organ

It’s already known that hormones could affect bones. Menopausal women experience dramatic drops in estrogen production; hence they are more prone to suffer from osteoporosis, said Ferron, the director of the Integrative and Molecular Physiology Research Unit at IRCM.

The recent discovery of osteocalcin, shed light on the concept that bone itself could affect other tissues. The hormone facilitates the metabolism of sugar. Osteocalcin increases the release of insulin, which in turn decrease the blood glucose levels. It also promotes the energy utilization and thereby protects the body from obesity, Ferron noted.

Previous studies have shown that, in some individuals, changes in blood concentrations of osteocalcin may even ward off diabetes. These protective features sparked Ferron's interest in how this hormone works.

Hormone scissors

Osteocalcin is secreted by osteoblasts, which is responsible for the synthesis of bones. The hormone builds up in bone, after a series of chemical reactions, is released into the blood. Hence the research team focused on this crucial step.

Ferron said osteocalcin are inactive when they are first produced in osteoblasts. "What interested us was understanding how osteocalcin becomes active to be able to play its role when released into the blood.”

The Study demonstrated that an enzyme is required, which acts like molecular scissors. Inactive osteocalcin has one more piece than active osteocalcin. The team assessed in mice the different enzymes present in cells where osteocalcin was produced that could be responsible for snipping off the piece in question.

The researchers succeeded to find a protein molecule, called furin that helps to activate the osteocalcin, and then release into the blood. According to the Ferron, when there is no furin in bone cells, inactive osteocalcin builds up and release, but this lead to an elevation in blood glucose levels and a reduction in energy expenditure as well as insulin release.

The removal of those scissors also exhibited an unexpected effect: it caused the lack of the appetite in mice. “We're confident that the absence of furin was the cause,” said Ferron.

The study findings suggest the presence of a new bone hormone that regulates food intake, Ferron noted. In future, the researchers are intended to determine whether furin interacts with another protein involved in regulation of appetite. The present discovery would open the innovative ways to prevent type-2 diabetes and obesity.