摘要
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: This study was to reveal the molecular mechanism of type Ⅱ diabetes and the protective effect of glutamine. [WT5FZ]Methods: C 57 BL/6 J mice were raised on high fat diet and the insulin receptor was studied by using the radioligand binding assay. [WT5FZ]Results: (1) The number of insulin receptor in hepatocytic and muscular membrane was reduced significantly in mice fed high fat diet compared with that of control. (2) The affinity of insulin receptor was also lower in mice fed high fat diet. Glutamine could prevent the decreasing tendency in the number and affinity of insulin receptor induced by high fat diet to some extent. [WT5FZ]Conclusion: Changes of the number of insulin receptor and affinity might be one of the key mechanisms in type Ⅱ diabetes development induced by high fat diet. Glutamine may protect mice from diabetes through restoration of the number of insulin receptor and its affinity.
出处
《营养学报》
CAS
CSCD
北大核心
2000年第2期163-165,共3页
Acta Nutrimenta Sinica
基金
中国科学院上海生物化学研究所分子生物学国家重点实验室经费资助
