(Ivanhoe Newswire) -- The loss of insulin-producing beta cells in the
pancreas is known to lead to diabetes. In people with the type 1 form of the
condition, 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.
SOURCE: Cell Metabolism, published online February 3, 2009
