US scientists have shown that a single protein plays a central co-ordinating role in the development of diabetes.
Pancreas cells produce the hormone insulin
A Stanford University team found that calcineurin is key to the health of the insulin-producing pancreatic beta cells that are defective in diabetes.
A study on mice showed the protein regulates 10 genes that had already been associated with the condition.
The Nature study raises hope of new treatments for a condition which affects millions worldwide.
In diabetes, the beta cells produce too little insulin or none at all, which prevents cells of the body from being able to take in sugar after a meal.
Sugar accumulates in the blood, damaging the blood vessels, kidneys and eyes.
The fact that immune-suppressing drugs, such as those taken by people undergoing transplant operations, greatly increase the risk of diabetes alerted the Stanford team to calcineurin.
The drugs are known to put a stranglehold on the protein.
Protein production stopped
The researchers worked with mice bred to produce calcineurin in the pancreas only until they were born.
After birth, the pancreas in each mouse stopped producing the protein.
By 12 weeks of age, the mice, which had been born with a normal number of beta cells, were severely diabetic.
Cutting the supply of calcineurin was found to prevent the beta cells from increasing their numbers as the mice grew - more body mass requires more beta cells to keep blood sugar in check.
It also reduced the amount of insulin made by the existing beta cells.
Researcher Dr Jeremy Heit said: "This work has led us and others to think in entirely new ways about diabetes.
"Until now people had identified individual genes or processes that were involved in diabetes.
"The new findings show that these lines of research are connected through a common regulator in calcineurin."
Next, the Stanford team bypassed calcineurin by artificially activating its protein sidekick, called NFAT.
Beta cells lacking calcineurin but with active NFAT behaved normally, multiplying as the mice aged and producing normal amounts of insulin.
The researchers said drugs that enhance the activity of calcineurin or NFAT could become a new treatment for type-2 diabetes, in which the beta cells do not produce enough insulin.
Drugs that inhibit calcineurin or NFAT may also treat diseases in which the beta cells produce too much insulin, such as hypoglycaemia or some pancreatic tumours.
Treating isolated beta cells with drugs that enhance calcineurin could make those cells divide, producing more cells for transplantation.
And activating calcineurin could potentially enable scientists to direct embryonic stem cells to become insulin-producing cells.
Dr Scott Campbell, vice president of research for the American Diabetes Association, said: "This work has the potential to be big.
"This is a step in the right direction and a major leap forward, but now we need to take it into humans."
Dr Angela Wilson, director of research at Diabetes UK, said: "This is a very interesting study.
"The prospect of novel drugs that could help to treat type 2 diabetes is welcome news given the epidemic numbers of people now developing the condition.
"This research is, however, at an early stage and the findings relate to mice. We look forward to seeing its relevance in humans."