last updated April 2013
Dialing up diabetes
Discovery of a mechanism that triggers inflammation in patients with type 2 diabetes could lead to a new type of treatment
An international team of researchers from Ireland, the USA and Japan has identified the protein islet amyloid polypeptide (IAPP), which is found in abnormal clumps in the pancreas of diabetic patients, as the cause of an increase of a regulator of the immune system that plays an important role in inducing diabetes. The regulator, proinflammatory cytokine interleukin-1β (IL-1β), increased when the team stimulated pancreatic immune cells with IAPP1.
The team found that mice that were expressing high levels of IAPP and on a high-fat diet — a significant risk factor for the development of diabetes in humans — also exhibited elevated levels of IL-1β.
The researchers showed that the clumps of IAPP are engulfed by the immune cells of the pancreas. This led to activation of a protein complex called the inflammasome, which was already known to be involved in the generation of IL-1β. In cells lacking portions of the inflammasome complex, they found that IAPP was unable to alter IL-1β protein levels.
Interestingly, a drug currently used to treat diabetes also inhibited IL-1β production that was induced by IAPP in the immune cells. The research team argues that reducing IAPP-induced activation of the inflammasome may be a new way to treat diabetes.
