摘要
铬可以提高动物机体组织对胰岛素的敏感性,但对其具体作用机制直到最近才有了较深入的认识.铬在吸收后主要由转铁蛋白运输.血液胰岛素水平升高可以促进转铁蛋白受体从细胞内的小泡中移位到细胞膜上.携带铬的转铁蛋白与细胞膜表面的转铁蛋白受体发生结合,通过内吞作用将铬转运到细胞内.在细胞内,内吞小泡中的酸性环境可使铬从转铁蛋白中释放,4个三价铬离子与apochromodulin形成有活性的holochromodulin.Holochromodulin除了可与胰岛素和/或胰岛素受体直接结合起作用外,还可以通过激活AMPK激酶来降低细胞膜胆固醇含量,改善细胞骨架功能,促进GLUT4移位,然后又通过激活p38MAPK激酶增强GLUT4的内在活性,从而促进葡萄糖吸收.但其具体分子机制仍不完全清楚.本文就铬在提高动物机体组织对胰岛素的敏感性的作用机制问题进行综述.
The chromium improves tissue sensitivity to insulin. However, the mechanisms underlying this process have not been known. Absorbed chromium in circulation mainly binds to transferrin. An increase in blood insulin concentration stimulates the transport of transferrin receptors from the vesicles inside ceils to the plasma membrane, where it binds to chromium-saturated transferrin, leading to endocytosis accompanied by Cr release at the acidic pH of the newly formed vesicles. Four Cr3. are sequestered by apochromodulin to produce active chromium-loaded holochromodulin. In addition to binding to insulin and/or insulin receptor directly to carry out its function, hopochromodulin also decreases cholesterol concent in plasma membrane by activating AMPK and thus improves the function of cytoskeleton to facilitate GLUT4 translocation. In addition, hopochromodulin improves GLUT4 intrinsic activity by activating p38MAPK and thus helps transport glucose into cell. However, the detailed molecular mechanisms have not been clarified.
出处
《中国生物化学与分子生物学报》
CAS
CSCD
北大核心
2009年第7期608-614,共7页
Chinese Journal of Biochemistry and Molecular Biology
基金
国家重点基础研究发展规划(973计划,No.2004CB117502)~~
