Diabetes is a widespread healthproblem, affecting some 400 million people across the planet. Withthat number only set to rise, it's important that we find newtreatments as quickly as possible. Researchers at the University ofMontreal are making significant progress in that regard, discoveringa common genetic defect in beta cells that may be a big factor inboth Type 1 and Type 2 diabetes.
Diabetes is caused by the body'sinability to lower blood glucose levels – something that's usuallyhandled by insulin. Type 1 patients' immune systems kill off the betacells that produce the insulin in the first place, while the liversof Type 2 sufferers are unable to properly process it. If leftuntreated, the condition can be extremely dangerous, resulting inblindness or even death.
In the past, researchers have looked atthe effects of genetics in altering the immune system in Type 1diabetes, and on metabolic dysfunction of the liver in Type 2. Thenew research pushed forward our understanding of the disease, findingthat genetics also affect the insulin-producing beta cells.
Working with laboratory mice, the teamfound that animals with weak beta cells that were ineffective atrepairing DNA damage quickly developed the disease when undercellular stress. Those with stronger cells that were good atrepairing DNA damage never developed the condition, even when thebeta cells were placed under severe levels of stress. The same trendwas observed when the researchers looked at the disease in human patients' samples, stronglyindicating a genetic predisposition for fragile beta cells heightensthe likelihood of developing the disease.
While the new information doesn'tdirectly translate to a new treatment, its thought that the breakthrough inunderstanding will drive the design of novel strategies for tacklingthe condition, such as new antidiabetic drugs that focus onpreserving beta cells.
The findings of the work were publishedonline in the journal Nature Genetics.
Source: University of Montreal