Diabetes is a widespread health problem, affecting some 400 million people across the planet. With that number only set to rise, it's important that we find new treatments as quickly as possible. Researchers at the University of Montreal are making significant progress in that regard, discovering a common genetic defect in beta cells that may be a big factor in both Type 1 and Type 2 diabetes.

Diabetes is caused by the body's inability to lower blood glucose levels – something that's usually handled by insulin. Type 1 patients' immune systems kill off the beta cells that produce the insulin in the first place, while the livers of Type 2 sufferers are unable to properly process it. If left untreated, the condition can be extremely dangerous, resulting in blindness or even death.

In the past, researchers have looked at the effects of genetics in altering the immune system in Type 1 diabetes, and on metabolic dysfunction of the liver in Type 2. The new research pushed forward our understanding of the disease, finding that genetics also affect the insulin-producing beta cells.

Working with laboratory mice, the team found that animals with weak beta cells that were ineffective at repairing DNA damage quickly developed the disease when under cellular stress. Those with stronger cells that were good at repairing DNA damage never developed the condition, even when the beta cells were placed under severe levels of stress. The same trend was observed when the researchers looked at the disease in human patients' samples, strongly indicating a genetic predisposition for fragile beta cells heightens the likelihood of developing the disease.

While the new information doesn't directly translate to a new treatment, its thought that the breakthrough in understanding will drive the design of novel strategies for tackling the condition, such as new antidiabetic drugs that focus on preserving beta cells.

The findings of the work were published online in the journal Nature Genetics.