Anti-inflammatory Cytokine Prevents Development of Insulin Resistance in Model

The anti-inflammatory cytokine interleukin 10 (IL-10) was found to prevent the age-related development of insulin resistance in the muscles of a genetically engineered mouse model.

Skeletal muscle is a major site of glucose disposal, and the role of aging-associated inflammation in skeletal muscle insulin resistance remains unclear. To investigate the connection between inflammation and insulin resistance, investigators at the University of Massachusetts Medical School (Worcester, USA) examined glucose metabolism in 18-month-old mice that were genetically engineered to overexpress IL-10 in their muscles and in their wild type counterparts.

The investigators reported in the November 3, 2016, online edition of The FASEB Journal that despite similar fat mass and energy balance, the genetically engineered mice were protected from aging-associated insulin resistance with significant increases in glucose infusion rates, whole-body glucose turnover, and skeletal muscle glucose uptake, as compared to age-matched wild type mice. This protective effect was associated with decreased muscle inflammation, but no changes in adipose tissue inflammation in the aging genetically engineered mice.

These results demonstrated the importance of skeletal muscle inflammation in aging-mediated insulin resistance, and further implicated a potential therapeutic role for anti-inflammatory cytokines in the treatment of aging-mediated insulin resistance.

"I hope that our research findings provide important new insights into the pathogenesis of insulin resistance that develops in aging and, more importantly, shed new light toward therapeutic potential of anti-inflammatory cytokines in the treatment of aging-associated metabolic and muscle diseases," said senior author Dr. Jason K. Kim, professor of molecular medicine at the University of Massachusetts Medical School.

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