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Your bones affect your appetite and metabolism, finds study

According to researchers, a hormone produced by our bones, called osteocalcin, affects how we metabolise sugar and fat.

fitness Updated: Nov 01, 2017 17:19 IST
The discovery may someday open the door to new ways of preventing type 2 diabetes and obesity.
The discovery may someday open the door to new ways of preventing type 2 diabetes and obesity.(Shutterstock)

Your skeleton is much more than the structure supporting your muscles and other tissues, it affects your appetite and metabolism too, a study has found.

Researchers from the Montreal Clinical Research Institute (IRCM) in Canada studied a hormone produced by our bones, called osteocalcin, which affects how we metabolise sugar and fat.

They unveiled a new piece of the puzzle that explains how osteocalcin works. The discovery may someday open the door to new ways of preventing type 2 diabetes and obesity.

It has long been known that hormones can affect bones, researchers wrote in the study published in The Journal of Clinical Investigation.

“Just think about how women are more prone to suffer from osteoporosis when they reach menopause because their oestrogen levels drop,” said Mathieu Ferron, director of the IRCM’s Integrative and Molecular Physiology Research Unit.

However, the idea that bone itself can affect other tissues took root only a few years ago with the discovery of osteocalcin. Thanks to this hormone, produced by bone cells, sugar is metabolised more easily.

“One of osteocalcin’s functions is to increase insulin production, which in turn reduces blood glucose levels,” Ferron said.

“It can also protect us from obesity by increasing energy expenditure,” he said.

Studies have shown that, for some people, changes in blood concentrations of osteocalcin may even stave off the development of diabetes.

Osteocalcin is produced by osteoblasts, the same cells responsible for making our bones.

The hormone builds up in bone, and then, through a series of chemical reactions, is released into the blood, researchers said.

“When it is first produced in osteoblasts, osteocalcin is in an inactive form,” Ferron noted.

“What interested us was understanding how osteocalcin becomes active so as to be able to play its role when released into the blood,” he said.

The researchers demonstrated that an enzyme, which acts like molecular scissors, is required. Inactive osteocalcin has one more piece than active osteocalcin.

They examined in mice the different enzymes present in cells where osteocalcin was produced that could be responsible for snipping off the piece in question.

Ferron’s team succeeded in identifying it: furin. It causes osteocalcin to become active and the hormone is then released into the blood.

“We demonstrated that when there was no furin in bone cells, inactive osteocalcin built up and was still released, but this led to an increase in blood glucose levels and a reduction in energy expenditure and insulin production,” Ferron said.

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