To determine if islet production of IL-1b was caused by the interaction of NLRP3 and TXNIP, the researchers exposed islet cells from normal mice and from mice deficient in NLRP3 or TXNIP to high glucose levels. As predicted, the protein-deficient islets made less IL-1b.
What's more, these deficient mice cleared glucose from the bloodstream quicker in response to insulin.
"Our findings predict that type 2 diabetes can be treated by inhibitors of the inflammasome or IL-1b," Tschopp said.
The good news is that these effects of NLRP3 are confined to the insulin-producing beta cells of the pancreas, so compounds to inhibit the pathway should not have systemic effects.
Studies in humans are already under way. According to Tschopp, "clinical studies with type 2 diabetes patients have already been initiated and the first results are again incredibly encouraging. With a single injection of IL-1b inhibitors, glucose levels in diabetes patients are highly reduced during six months. This treatment could replace the standard treatment currently used."'
There's more on type 1 and type 2 diabetes at the American Diabetes Association.
SOURCES: Jurg Tschopp, Ph.D., professor, University of Lausanne, Epalinges, Switzerland; Norma Kenyon, M.D., Martin Kleiman professor of surgery, medicine, microbiology and immunology and biomedical engineering, Diabetes Research Institute, University of Miami Miller School of Medicine; Dec. 21, 2009, online Nature Immunology
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