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JNK genes key to obesity-induced diabetes

Blocking the body’s inflammatory response to high-fat foods may prevent people with obesity from becoming insulin resistant, according to a new study.
The research, published online in the journal Science, found that the JNK signalling pathway in mice contributes to inflammation and plays a key role in the metabolic response to obesity, including insulin resistance, a precursor to type 2 diabetes.
By switching off this pathway in mice fed a high-fat diet, they authors found that the rodents became obese but remained insulin sensitive, as opposed to mice given the same diet with intact JNK pathways.
“What we discovered is the JNK genes in the macrophages [white blood cells that fight infection] are critical for the ability of macrophages to cause inflammation, specifically in response to feeding or eating a high-fat diet,” said study author Roger Davis.
He explained that the absence of JNK genes in the macrophages prevents this inflammatory response, which “in turn prevents the development of symptoms of pre-diabetes, like insulin resistance”.
Davis, a professor at the University of Massachusetts Medical School and investigator at the Howard Hughes Medical Institute, said there is the possibility that the animal research findings might apply to humans.
“One possible scenario – and obviously our work is on mice, so there’s a big leap of faith here to establish [this] in humans – but the work we’ve done would suggest that drugs that are targeted to JNK kinase genes would be useful for the treatment of diabetes,” he explained. “But this is definitely a big step beyond the point of our own work.”

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