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目的 研究 型糖尿病发生的分子机制及谷氨酰胺保护作用的可能机理。方法 以高脂饮食诱发 C 57BL/ 6J小鼠 型糖尿病 ,观察肝、骨骼肌细胞膜对胰岛素特异结合及谷氨酰胺的影响。结果 1 .高脂饮食诱发的 型糖尿病小鼠其肝、骨骼肌细胞膜受体数均较正常对照组减少 ,谷氨酰胺有抑制其受体数目减少的趋势。 2 .糖尿病小鼠肝、骨骼肌胰岛素受体亲和力明显降低 ,而谷氨酰胺可在一定程度上提高其亲和力。结论 胰岛素受体数目及亲和力的改变可能是高脂诱发 型糖尿病的重要机制之一 ,而谷氨酰胺也可能是通过恢复机体胰岛素受体数目和亲和力而对 型糖尿病有一定的防治作用。
Objective To study the molecular mechanism of diabetes and the possible mechanism of glutamine protection. Methods C57BL / 6J mice were induced with high fat diet to observe the effects of liver and skeletal muscle cell membrane on insulin-specific binding and glutamine. Results 1. The number of receptor of liver and skeletal muscle cell membrane in diabetic mice induced by high-fat diet was decreased compared with that of normal control group, and glutamine had a tendency of decreasing the number of its receptor. The affinity of insulin receptor in liver and skeletal muscle of diabetic mice was significantly reduced, but glutamine could improve its affinity to a certain extent. Conclusion The changes of insulin receptor number and affinity may be one of the important mechanisms of hyperlipidemic diabetes. Glutamine may also have some preventive and therapeutic effects on type diabetes by restoring the number and affinity of insulin receptors in the body.