摘要
目的:从胰岛素信号转导方面研究α-亚麻酸对胰岛素抵抗的作用及可能的机制,为富含α-亚麻酸的植物油应用于糖尿病的防治提供实验依据。方法:原代培养大鼠骨骼肌细胞,应用免疫印迹法检测α-亚麻酸对大鼠骨骼肌细胞蛋白激酶B(PKB)信号转导通路及葡萄糖转运蛋白4(GLUT4)表达的影响。结果:在0.125-1.0μmol/L的浓度范围,α-亚麻酸对骨骼肌细胞PKB的磷酸化及GLUT4蛋白的水平呈剂量一效应关系及时间-效应关系,对PKB的表达水平未见影响;采用P13K抑制剂LY294002(15μmol/L)抑制P13K/PKB信号通路后,GLUT4蛋白水平、PKB磷酸化同空白对照相比较均无显著性差别(P>0.05)。结论:α-亚麻酸通过作用于肌细胞胰岛素的P13K/PKB信号通路,进而调节GLUT4的蛋白表达水平,增加骨骼肌对胰岛素的敏感性,减轻或避免骨骼肌胰岛素抵抗和糖代谢障碍。
Objective: To study the effect of a-linolenic acid on insulin resistance and its mechanism concerning the insulin signal transduction,providing a theoratic basis for applying plant oil rich in a-linolenic acid in preventing and treating diabetes. Methods :The effect of a-linolenic acid on protein kinase B(PKB) signal transduction and expression of glucose transport protein 4(GLUT4) in rat skeletal muscles was detected by primary cell culture and Western blot techniques. Results:At the concentration of 0. 125-1. 0μmol/L, a-linolenic acid promoted the PKB phosphorylation, but didnot influence the expression of PKB. The expression of GLUT4 protein was dose-dependent and time-dependent. Adding PI3K inhibitor LY294002(15 μmol/L) in a-linolenic acid cultured skeletal muscle cells made no significant difference in the level of PKB phosphorylation and GLUT4 protein. Conclusion:a-linolenic acid can improve the level of GLUT4 protein by promoting skeletal muscle PI3K/ PKB signal transduction,and increase the sensitivity of skeletal muscle on insulin, which can alleviate or avoid insulin resistance and glycometabolic disturbance.
出处
《第二军医大学学报》
CAS
CSCD
北大核心
2003年第11期1219-1221,共3页
Academic Journal of Second Military Medical University