We’ve long been told that a part of our brain controls our appetite – but a new study suggests that our bones also play a key role.
A hormone they produce, called osteocalcin, has been shown to affect how we metabolise sugar and fat.
It has also been associated with insulin sensitivity, which is linked to developing type 2 diabetes.
Previous research already uncovered this, and now Canadian researchers have unveiled a new piece of the puzzle – they believe they have identified the protein which causes osteocalcin to activate.
They hope their findings will open the door to new ways of preventing type 2 diabetes and obesity.
We know a hormone produced by the bones called osteocalcin is linked to our appetites and metabolism – now a new study has revealed how it is triggered (stock photo)
Professor Mathieu Ferron, of the Montreal Clinical Research Institute (IRCM), spent the last decade studying osteocalcin.
He says it has long been known that hormones can affect bones, adding: ‘Just think about how women are more prone to suffer from osteoporosis when they reach menopause because their oestrogen levels drop.’
But he said the idea that bone itself can affect other tissues took root only a few years ago.
‘One of osteocalcin’s functions is to increase insulin production, which in turn reduces blood glucose levels,’ he said.
‘It can also protect us from obesity by increasing energy expenditure.’
Studies have shown that, for some people, changes in blood concentrations of osteocalcin may even stave off the development of diabetes.
The protective properties sparked the team’s interest in how the hormone actually works.
Key findings
Professor Ferron says 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. The researchers have focused on this key step.
‘When it is first produced in osteoblasts, osteocalcin is in an inactive form,’ he explained.
‘What interested us was understanding how osteocalcin becomes active so as to be able to play its role when released into the blood.’
His lab demonstrated that an enzyme, which acts like molecular scissors, is required. Inactive osteocalcin has one more piece than active osteocalcin.
The researchers examined in mice the different enzymes present in cells where osteocalcin was produced that could be responsible for snipping off the piece in question.
Canadian researchers hope their discovery of how bone hormone osteocalcin works will lead to new therapies to prevent type 2 diabetes and obesity (stock photo)
Professor Ferron’s team succeeded in identifying the protein furin which causes osteocalcin to become active and the hormone is then released into the blood.
He said: ‘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.’
Professor Ferron explained that deleting these ‘scissors’ also had an unexpected effect: it reduced the mice’s appetite.
He said: ‘We’re confident that the absence of furin was the cause.’
His team showed that osteocalcin itself has no direct effect on appetite.
Prof Ferron added: ‘Our results suggest the existence of a new bone hormone that controls food intake.
‘In future work, we hope to determine whether furin interacts with another protein involved in appetite regulation.’
The findings were published in The Journal of Clinical Investigation.