JNK1 ablation in mice confers long-term metabolic protection from diet-induced obesity at the cost of moderate skin oxidative damage.

摘要: Obesity and insulin resistance are associated with oxidative stress, which may be implicated in the progression of obesity-related diseases. The kinase JNK1 has emerged as a promising drug target for treatment obesity type 2 diabetes. is also key mediator stress response, can promote cell death or survival, depending on magnitude context its activation. In this article, we describe study long-term effects inactivation glucose homeostasis obese mice were investigated first time. Mice lacking (JNK1(-/-)) fed an obesogenic high-fat diet (HFD) long period. JNK1(-/-) HFD term had reduced expression antioxidant genes their skin, more skin damage, increased epidermal thickness inflammation compared control wild-type mice. However, observed that protection from obesity, adipose tissue inflammation, steatosis, resistance, conferred by ablation, was sustained over period paralleled decreased damage fat liver. We conclude compounds targeting activity brain tissue, do not accumulate safer most effective.-Becattini, B., Zani, F., Breasson, L., Sardi, C., D'Agostino, V. G., Choo, M.-K., Provenzani, A., Park, J. M., Solinas, G. ablation confers metabolic diet-induced at cost moderate damage.