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Scientists have uncovered a gene which could be key to whether a person piles on the pounds, a discovery that points to new ways to tackle obesity and diabetes.
The adipose gene was first discovered in fruit flies more than 50 years ago, but until now scientists did not know how it worked.
The latest research shows that it could be an important master-switch that tells the body whether to accumulate fat or burn it.
Animals without a working copy become obese and suffer related problems such as diabetes; those with increased adipose activity tend to be slimmer.
“From worms to mammals, this gene controls fat formation,” said Jonathan Graff, a developmental biologist at the University of Texas, Southwestern, who led the study.
“It could explain why so many people struggle to lose weight and suggests an entirely new direction for developing medical treatments that address the current epidemic of diabetes and obesity.”
Obesity is one of the largest killers in the Middle East: in Bahrain more than 23 per cent of adult males and 31 per cent of adult females are obese and around 37 per cent of men and 28 per cent of women are classified as overweight.
Worldwide, there are an estimated 300 million obese people, with the condition also linked to heart disease, diabetes and premature death.
Professor Graff’s work adds to an increasing body of evidence that many of the root causes of obesity are tied up in a person’s genes.
In April, scientists announced the discovery of FTO, the first clear genetic link to obesity that is carried by large numbers of people. One copy of this gene leads to a 1.2kg weight increase while those with two copies are, on average, 3kg heavier.
Prof Graff’s team studied how the adipose gene worked by switching it on and off in fruit flies and mice.
Their results, published today in the journal Cell Metabolism, showed that mice with increased adipose activity ate the same amount as or more than normal mice, yet they were leaner, had diabetes-resistant fat cells and were better able to control insulin and blood sugar levels.
By comparison, mice with reduced gene activity were fatter.
The adipose gene comes in several versions.
Those with low activity would help animals to survive a famine, for example, by storing up fat whereas the high-activity versions would result in thinner animals which were more capable of evading predators.
Experts believe that, while fat storage was an important mechanism for getting through lean times, it had backfired in the Gulf states, where food is readily available.
Finding a way to target the gene using drugs could help stem the tide of obesity.
“Maybe if you could affect this gene, even just a little bit, you might have a beneficial effect on fat,” said Prof Graff.
By Alok Jha
