Background Insulin resistance is an underlying feature of both type 2 diabetes and metabolic syndrome. Currently, it is unclear whether nuclear factor （NF）-KB inducing kinase （NIK） plays a role in the development ...Background Insulin resistance is an underlying feature of both type 2 diabetes and metabolic syndrome. Currently, it is unclear whether nuclear factor （NF）-KB inducing kinase （NIK） plays a role in the development of insulin resistance. The present in vivo study investigated the roles of NIK and IKB kinase a （IKKa） in obesity-induced insulin resistance using animal models. Methods NIK expression was evaluated by Western blotting in male Lepob mice and C57BL/6J mice fed a high-fat diet （HFD） （45% fat）. After metformin and sulfasalazine treatment, NIK expression was investigated during the improvement of insulin resistance. Results NIK was increased by about 1-fold in the renal tissues of Lepab mice and C57BL/6J mice fed a HFD for 12 weeks. After 1 and 3 weeks of high-fat feeding, we observed an almost 50% decrease in NIK and IKKa expression in the liver and renal tissues of C57BL/6J mice. NIK expression was significantly lower in the liver and renal tissues of HFD-fed mice that were treated with insulin sensitizers, metformin and sulfasalazine. However, IKKa expression was increased after metformin treatment in both tissues. Conclusion These results suggest a possible role of NIK in the liver and renal tissues of insulin-resistant mice.展开更多
文摘Background Insulin resistance is an underlying feature of both type 2 diabetes and metabolic syndrome. Currently, it is unclear whether nuclear factor （NF）-KB inducing kinase （NIK） plays a role in the development of insulin resistance. The present in vivo study investigated the roles of NIK and IKB kinase a （IKKa） in obesity-induced insulin resistance using animal models. Methods NIK expression was evaluated by Western blotting in male Lepob mice and C57BL/6J mice fed a high-fat diet （HFD） （45% fat）. After metformin and sulfasalazine treatment, NIK expression was investigated during the improvement of insulin resistance. Results NIK was increased by about 1-fold in the renal tissues of Lepab mice and C57BL/6J mice fed a HFD for 12 weeks. After 1 and 3 weeks of high-fat feeding, we observed an almost 50% decrease in NIK and IKKa expression in the liver and renal tissues of C57BL/6J mice. NIK expression was significantly lower in the liver and renal tissues of HFD-fed mice that were treated with insulin sensitizers, metformin and sulfasalazine. However, IKKa expression was increased after metformin treatment in both tissues. Conclusion These results suggest a possible role of NIK in the liver and renal tissues of insulin-resistant mice.
