The Influence And Mechanisms Of Selenite On Insulin Signaling Pathway In High-Fat Diet-Fed Type2Diabetic Mice

Selenium is an essential micronutrient in mammals. Selenium was found to haveseveral insulin-like effects. Recent studies show that low selenium and high selenium bothincrease the incidence of type2diabetes. However the internal mechanism is stillunknown or poorly understood. A large number of studies have shown that insulinresistance holds an extremely important position in the pathogenesis of type2diabetes.Thus, studies of the relationship between selenium and insulin resistance will be beneficialto further understand the biological functions of selenium, and may provide someinformation for the prevention and treatment of type2diabetes.In this paper, the role of selenite in promoting insulin resistance through the inductionof oxidative stress, activation of the ASK1-MKK4-JNK signaling pathway and inhibitionof IRS protein expression were examined in high-fat diet-fed type2diabetic mice andhigh-fat diet-fed mice. The main results are as follows:Insulin intolerance of selenite-treated diabetic mice was promoted in comparison todiabetic mice. Compared with diabetic mice, IRS1protein expression in liver wassignificantly decreased by selenite. Compared with diabetic mice, phosphorylation ofASK1, MKK4and JNK were all significantly increased by selenite. Compared withdiabetic mice, contents of malondialdehyde and protein carbonyl were both significantlyincreased by selenite. Experimental results consistent with the above. These resultsindicated that high-fat diet was the key factor that selenite promoted the development ofdiabetes.