Uncoupling protein 2 protects mice from aging

In this study, we examined the phenotype of aging in a large colony of Ucp2-deficient (Ucp2−/−) mice on the molecular level. We have found that the significantly shorter lives of Ucp2−/− mice is the result of an accelerated aging process throughout their entire lifespan. Thus, Ucp2−/− mice not only earlier gained sexual maturity, but also earlier progressed into an aging phenotype, reflected by a decrease in body weight, increased neutrophil numbers, and earlier emergence of spontaneous ulcerative dermatitis. Intriguingly, on the molecular level this acceleration in aging predominantly driven by increased levels of circulating IGF-1 in Ucp2−/− mice, hinting at a crosstalk between UCP2 and the classical Insulin/IGF-1 signaling aging pathway.