Inflammation Plays a Major Role in Diabetes

Beta cell failure in the pancreas leads to both type 1 and 2 diabetes.  Especially in people with Type 1 diabetes, these cells are killed by high concentrations of inflammatory signals, but scientists have been at a loss to explain how they are eliminated in people with the type 2 form of the disease.

New research is helping to answer the question. In a study involving cell samples taken from people with and without type 2 diabetes, investigators found more than 30 times the amount of an inflammatory factor called CXCL10 in people with diabetes. When they exposed human pancreatic cells to CXCL10 in the laboratory, beta cells were decreased in number, and the ability of the cells to make and secrete insulin declined.

The researchers went on to identify a key protein in the immune system pathway CXCL10 uses to achieve these effects on the pancreas. Now they believe they can use this protein, called TLR4, to find a way to stop the process.

"To prevent such a progression using anti-inflammatory targets of the TLR4 signaling pathway will be of high importance to rescue the beta cell from inflammation-induced self-destruction and [to] preserve beta cell function and mass," conclude the investigators.

Cell Metabolism, published online February 3, 2009