A newly identified protein involved in inflammation may be a key player in the induction of Type 2 diabetes (T2D), according to a report published online this week in Nature Immunology. Targeting the components of this inflammatory pathway may lead to new therapies for T2D ― a metabolic disease with rising incidence in the developed world.
Jurg Tschopp and colleagues found that TXNIP, a protein previously associated with insulin resistance, is intimately involved in switching on the NLRP3 inflammasome ― a complex of proteins that mediates production of the immune messenger, IL-1beta, and inflammation. Various stress or danger signals, such as infection, were found to release TXNIP from its bound inactive state, making it available for the activation of the NLRP3 inflammasome and IL-1beta release. Hyperglycemia ― an excess of sugar in the blood ― induces IL-1beta release from certain cells in a way which is dependent on TXNIP and therefore could be responsible for the mild chronic inflammation observed in diabetes.
This study provides a link between hyperglycemia and inflammation, and could lead to new effective therapies for T2D and other inflammatory diseases if methods are found to target components of the NLRP3 inflammasome.
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