Our skeleton is much more than the framework that supports the muscles and tissues of your body. It also acts as a hormone producer. Mathieu Ferron knows something about it. The researcher at the Montreal Clinical Research Institute (IRCM) and professor at the Faculty of Medicine of the Université de Montréal has been studying osteocalcin for the past decade. This hormone produced by our bones would influence the metabolism of sugar and fats in our body.
In a recent article published in The Journal of Clinical Investigation, the team of Dr. Ferron has also unveiled a new piece of the puzzle that explains the operation of osteocalcin. Ultimately, this discovery could open the door to avenues for preventing type 2 diabetes and obesity.
Bone, an endocrine organ
It has long been known that hormones can affect bones. “You only have to think about women who are more affected by osteoporosis when they reach menopause. It is because of the lowering of their level of estrogen that they are more prone,” says Ferron, director of the IRCM’s integrative and molecular physiology research unit.
However, the idea that the bone itself can act on other tissues made its way a few years ago with the discovery of osteocalcin, a hormone produced by the cells of the bone. Thanks to this one, our metabolism could more easily assimilate sugar.
“Osteocalcin helps, among other things, to produce insulin, which lowers the level of glucose in our blood. It could also protect us from obesity by increasing our energy expenditure, “explains Mathieu Ferron. Studies even indicate that changes in blood levels of osteocalcin may influence the development of diabetes in some people. These protective properties aroused Ferron’s curiosity. This is why he is interested in the mechanisms that govern the functioning of this hormone.
Osteocalcin is made by the same cells that are responsible for forming our bones, osteoblasts. It then accumulates inside the bone. Then, thanks to a succession of chemical reactions, the hormone is released in the blood. It is also on this decisive stage that the team of the IRCM has looked.
“When produced in osteoblasts, osteocalcin is initially inactive,” says Ferron. What interested us in this study was to understand how the hormone became active in order to play its role when released into the bloodstream. ”
The IRCM laboratory has succeeded in demonstrating the need to use an enzyme that acts as a molecular chisel. Indeed, osteocalcin in its inactive form is provided with a piece of more than in its active form. The researchers therefore examined in the mouse the different enzymes present in the cells where the osteocalcin was made and which could be likely to cut the piece in question. The team of Ferron came to designate the great responsibility: furin. With the latter, the osteocalcin becomes active and then released into the blood.
“We demonstrated that, in the absence of furin in bone cells, the inactive form of osteocalcin accumulated and was released,” says Mathieu Ferron. However, this has the effect of increasing the level of glucose in the blood, reducing energy expenditure and reducing insulin production.”
The removal of this famous “scissors” in bone cells has also had an unexpected effect: a decrease in appetite in mice.
“We are convinced that it is the absence of fur that is the cause,” says Ferron. His team has actually shown that osteocalcin itself has no effect on appetite. “Our results show the existence of a new bone hormone controlling food intake. In our next work, we will therefore want to check if the furine would not interact with another protein involved in the regulation of appetite,” concludes the researcher.
The British Journal Editors and Wire Services