论文部分内容阅读
目的 探讨糖皮质激素和高浓度糖 (高糖 )共同作用诱导胰岛素抵抗的分子机理。方法 分离的大鼠脂肪细胞在 5 2 5mM葡萄糖或加地塞米松 (Dex) 0 3μM培养基中孵育 2 4h ,然后测定葡萄糖的转运率 ,胰岛素受体底物 (IRS) 1/ 2的酪氨酸磷酸化、IRS 1/ 2及蛋白激酶B(PKB)的蛋白表达。结果 高糖抑制了这些细胞的糖摄取率、IRS1酪氨酸磷酸化及蛋白表达 ,Dex加重高糖的以上抑制作用 ;高糖增加IRS2蛋白表达 ,Dex部分对抗高糖的此作用及抑制IRS2酪氨酸磷酸化。结论 高糖能诱导胰岛素抵抗 ,Dex加重高糖的此作用。其作用机制与影响胰岛素信号蛋白磷酸化及蛋白表达等因素有关。
Objective To investigate the molecular mechanism of insulin resistance induced by glucocorticoid and high concentration of sugar (high glucose). Methods Rat adipocytes isolated were incubated for 24 hours in 5 2 5 mM glucose or dexamethasone 0 3 μM medium and then assayed for glucose transport rate, insulin receptor substrate (IRS) 1/2 tyrosine Phosphorylation, IRS 1/2 and protein kinase B (PKB) protein expression. Results High glucose inhibited the uptake of glucose, IRS1 tyrosine phosphorylation and protein expression, Dex aggravated the above inhibition of high glucose. High glucose increased the expression of IRS2 protein, Dex partially antagonized the effect of high glucose and inhibited IRS2 Amino acid phosphorylation. Conclusion High glucose can induce insulin resistance, Dex aggravates the effect of high glucose. Its mechanism is related to factors such as insulin signaling protein phosphorylation and protein expression.