They have found that, contrary to popular belief, body fat can in fact be of benefit, boosting the body’s ability to regulate blood sugar.
Experts now hope the discovery could pave the way for a new treatment for type 2 diabetes.
Nearly three million people in the UK have been diagnosed with diabetes and 850,000 have the condition without knowing it.
The majority – around 2.5 million – have type 2 diabetes, which can cause strokes, heart attacks and blindness.
This normally develops during middle age from obesity or an unhealthy lifestyle.
It differs from type 1 diabetes – which usually develops before the age of 40 and requires sufferers to take insulin injections – in that it can be prevented.
Now, researchers from Harvard Medical School in Boston, USA, have shown that the gene, called ChREBP, can actually prompt the body to resist diabetes by converting glucose sugar into fatty acids.
The general concept of fat as all bad is not true
It also boosts sensitivity to insulin, the vital hormone that regulates blood sugar.
In most obese people, sugar is blocked from entering fat cells and blood sugar levels rise.
Eventually, this leads to insulin resistance and type 2 diabetes.
The findings add to previous research based on 123 fat samples from non-diabetic people which showed the gene was more active in those whose bodies had a better sugar balance. The gene’s activity also correlated with insulin sensitivity in obese, non-diabetic people.
Lead investigator Dr Mark Herman, said: “The general concept of fat as all bad is not true.
“Obesity is commonly associated with metabolic dysfunction that puts people at higher risk for diabetes, stroke and heart disease, but there is a large percentage of obese people who are metabolically healthy.
“We started with a mouse model that disassociates obesity from its adverse effects.”
Dr Herman’s team tweaked a “glucose transporter” gene in obese mice that serves as a gateway for sugar. Usually, its activity in fat cells drops with obesity.
The scientists found that when they increased glucose transporter levels in obese mice – allowing more sugar into their fat cells – they were protected against diabetes. Conversely, normal weight mice missing the glucose transporter gene developed diabetes symptoms.
The research showed sugar in fat cells triggered a response from the ChREBP gene that regulated insulin sensitivity throughout the body.
The findings appear in the online edition of the journal Nature.
Commenting on the study, Professor Ulf Smith, from the University of Gothenburg in Sweden, who is president of the European Association for the Study of Diabetes, said: “It’s a really exciting finding. We’ve been looking for the mechanism to try to understand why glucose metabolism in adipose tissue is so important for whole-body sensitivity to insulin.”
Eight years ago scientists learned that when fat cells start to have trouble taking in sugar, it can be an early indicator of diabetes.
In healthy people, fat cells normally take up around 10 per cent of the sugars derived from food.
The researchers wrote: “These data suggest that selective activation of adipose tissue ChREBP could be an effective therapeutic strategy for preventing and treating type 2 diabetes and obesity-related metabolic diseases.”