n a new study, researchers have shown that a protein called NLRP1 (nucleotide-binding domain and leucine-rich repeat containing family, pyrin domain ccontaining 1) (image) is switched on when increased dietary energy (food) intake triggers a cell to become "unstable." Activation of this protein sets off a chain of events that instructs cells to use up their fat stores to prevent excess fat accumulating. The new research, directed by Dr. Seth Masters from Melbourne's Walter and Eliza Hall Institute and Dr. Andrew Murphy and Dr. Michael Kraakman from the Baker IDI Heart and Diabetes Institute (also in Melbourne), with obesity expert Mark Febbraio from the Garvan Institute (in Sydney), was published online on October 22, 2015 in Cell Metabolism. The article is titled “IL-18 Production from the NLRP1 Inflammasome Prevents Obesity and Metabolic Syndrome.” Dr. Masters said that NLRP1 is a biological sensor that could hold the key to developing new ways of treating obesity and type 2 diabetes. "NLRP1 is a biological sensor that can respond to and prevent obesity and metabolic syndrome, which are causing a dramatically increasing burden of disease throughout the world," Dr. Masters said. "The sensor is activated if it detects that the body's energy intake is too high. When the sensor is activated, it tells cells to burn fat stores to prevent excess build-up of fat. We showed that without NLRP1, fat stores continue to build up, especially with a high-energy diet, leading to obesity." Dr. Masters said that NLRP1 has been more commonly known for its role in the immune system. "However it is becoming increasingly clear that immune signalling proteins also have an important role in regulating metabolism." Dr.
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