- German researchers say muscle loss and a fatter stomach are signs of ageing
- The team used a chemical to switch fat cell receptors linked to muscle and fat
- In mice triggering them encouraged body fat to burn and better muscle growth
Reversing physical ageing could be as simple as giving people a treatment that encourages their body to burn fat and promote muscle growth, study finds.
Researchers from the University of Bonn worked from the idea that a fatter stomach and shrinking muscles are common signs of ageing that ‘could be reversed’.
This treatment – which involves switching receptors that regulates weight and muscle growth – has so far only been tested on mice and in human cell cultures.
The German research team found that by triggering these receptors on a fast-burning form of fat, older mice become much fitter and as healthy as younger mice.
They then compared the fat cells and pathways in the mice with human cells and found they were essentially the same, meaning it should to do the same with people.
Researchers from the University of Bonn worked from the idea that a fatter stomach and shrinking muscles are common signs of ageing that ‘could be reversed’. Stock image
Researchers have been studying ways of converting flabby ‘white fat’ to this ‘brown fat’ – which the body tends to burn as an energy source – for years.
This new study is a breakthrough in the search to make that conversion possible and the team say brown fat has more A2B receptors than white fat.
This is the key to burning fat as energy, rather than leaving it lying dormant around our bellies and thighs, according to the team behind the discovery.
As they age, mice increasingly lose muscle mass – similar to humans and just like us, they also tend to gain a lot of fat around the hips over the years.
However, if they receive the chemical that activates the A2B receptor, these ageing effects are inhibited, according to the German team.
They then gave older mice treatment to activate their A2B receptors and found they did indeed start burning more fat similar to younger mice.
However, the impact went further as they did not lose weight but instead gained muscle, and the scientists found that muscles were also high in A2B receptors.
After four weeks of the treatment, the oxygen consumption of the mice had been boosted by almost 50 per cent, and they were found to have about as much muscle mass as young mice.
‘A2B activation can therefore reverse both ageing effects to a certain extent,’ said Thorsten Gnad, the lead author of the study.
To check whether the results might carry across to people, the team then examined human cells and discovered the same mechanism appeared to be at work.
The next stage will be to work out how to deliver such treatment safely to humans.
Professor Alexander Pfeifer, from the study team, said it had implications for tackling the body’s decline with age and battling health issues related to global obesity.
‘Obesity is a growing problem worldwide,’ said Pfeifer.
The German research team found that by triggering these receptors on a fast-burning form of fat, older mice become much fitter and as healthy as younger mice. Stock image
‘Every extra pound not only increases the risk of developing diabetes, but also the risk of high blood pressure, vascular damage and heart attacks and strokes.
‘These problems are further exacerbated by muscles that shrink over the years, as they further reduce the body’s energy requirements both at rest and in motion.’
The pharmacologists explain that the prospect of having a receptor on hand that might be able to slow down both of these age-related phenomena is highly exciting.
However, further research would first have to show to what extent the human mechanisms actually resemble those in mice.
Additionally, there is currently no activator of A2B approved for use in humans so little is known about any side effects of such a treatment.
‘We found no signs of adverse reactions in mice,’ says Pfeifer. ‘However, the meaningfulness of the results is, of course, also limited on this matter.’
The research was published in the latest edition of the scientific journal Cell Metabolism.