They say that overeating stimulates the conversion of oxygen into toxic free radicals, or oxidants, which stop the body using insulin properly.

That causes the pancreas to burn out, leading to diabetes.

The team from the Garvan Institute in Sydney says their findings are an important step to creating better treatments.

Professor David James from the Garvan Institute says it all takes place in the part of a cell called the mitochondria.

"If we eat the right amount of food, most of the nutrients get diverted into energy production and all is well," he said.

"But if we overeat, we can actually make the mitochondria oversupplied with nutrients and now instead of converting the nutrients to energy, they can start to convert the nutrients into oxidants."

Professor James says the oxidants then lead to insulin resistance.

"Where insulin is unable to do its job properly in muscle and fat cells, that in turn leads to pancreas oversecreting insulin in order to get the job done," he said.

"And so if that extra burden goes on and on and on for a long time, it can result in the pancreas essentially burning out."

That is diabetes, and for the moment, it is irreversible.

Natural defence mechanism

The scientists say that the body may be producing oxidants in the mitochondria as a natural defence mechanism.

"The signal says, I've had enough nutrients, please, no more," Professor James said.

"In fact, the insulin resistant mechanism may be a way that the cell tries to deal with that, to shut down an additional nutrient burden that accompanies overeating."

The findings mean that doctors may now be able to prevent the development of type two diabetes.

"One could easily imagine now developing anti-oxidants that will specifically target this particular place in muscle and fat cells," Professor James said.

He added that the antioxidants would have to take the form of specifically targeted drugs.

"There are lots and lots of antioxidants on the market," he said.

"You know, you can walk down the supermarket and there are loads and loads of them, but the problem I suspect with most of those is that they will not target the production of oxidants inside mitochondria."

The research is being published this week in the journal Proceedings of the National Academy of Sciences.

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