Switching off a single gene may allow people to eat whatever they want without getting fat, a study suggests.
In research on mice, experts from the University of California San Diego discovered that a single gene is responsible for fat cells losing their ability to burn energy.
They found that when rodents were fed a high-fat diet, their cells broke down and became less effective at burning fat – possibly explaining why obesity causes people’s metabolism to slow down.
The researchers discovered that this process is controlled by a single gene that, when removed via gene-editing, stopped the rodents from gaining excess weight, even while eating the same high-fat diet.
Switching off a single gene could allow you to eat whatever you want without getting fat, a study has suggested
The team wanted to examine how obesity affects our mitochondria and work out why being obese seems to slow down metabolism, making it easier to stay fat.
Dr Alan Saltiel, professor of medicine at UC San Diego and lead author of the study, said: ‘Caloric overload from overeating can lead to weight gain and also triggers a metabolic cascade that reduces energy burning, making obesity even worse.
‘The gene we identified is a critical part of that transition from healthy weight to obesity.’
When people are consuming more calories than they are burning, the ability of fat cells to burn energy begins to fail, which is one of the reasons it can be tricky for obese people to lose weight.
But how the fat cells start to fail has been one of obesity’s biggest mysteries.
The researchers measured the impact of a diet high in fat on mice’s mitochondria – the powerhouse of cells that aid fat-burning.
After eating the diet, the mice’s mitochondria fragmented into tinier, ineffective mitochondria that burned less fat.
This is achieved by a single gene called RaIA, which has many functions. One of them is helping break down mitochondria when they malfunction.
The researchers’ findings suggest that when this gene is overreactive, it gets in the way of mitochondria’s normal functioning, triggering fat cells to not burn energy as well.
Dr Saltiel said: ‘In essence, chronic activation of RaIA appears to play a critical role in suppressing energy expenditure in obese adipose tissue.
‘By understanding this mechanism, we’re one step closer to developing targeted therapies that could address weight gain and associated metabolic dysfunctions by increasing fat burning.’
The researchers found that some of the proteins affected by RaIA in mice are similar to human proteins that are linked to obesity and insulin resistance, suggesting that similar mechanisms may be at play in humans.
‘The direct comparison between the fundamental biology we’ve discovered and real clinical outcomes underscores the relevance of the findings to humans and suggests we may be able to help treat or prevent obesity by targeting the RaIA pathway with new therapies,’ said Dr Saltiel.
‘We’re only just beginning to understand the complex metabolism of this disease, but the future possibilities are exciting.’
Future treatments may involve gene therapies or CRISPR – a technology used by scientists to modify DNA in living beings – to get rid of RaIA and its effects in the body.
The study was published in the journal Nature Metabolism.
