2004年北京国际青光眼学术研讨会将于2004年4月8日 – 11日在北京召开。本次会议由中华医学会眼科学分会、世界眼科手术医师协会和中国医学会共同举办，欢迎大家踊跃投稿。
论文截稿日期：2004年1月３０日
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INSULIN-MEDIATED CELLULAR INSULIN RESISTANCE DECREASES SHOCK-INDUCED GLUCOSE TRANSPORT IN 3T3-L1 ADIPOCYTES
WANG Zhiwen, NIE Jianqiang, and LI Xiaoming
Department of Medicine, Division of Endocrinology and Metabolism, University of California, San Diego, La Jolla, USA
Objective: Similar to insulin, osmotic shock treatment of 3T3-Ll adipocytes causes an increase in glucose transport activity and translocation of GLUT-4 protein. In our study, we evaluated the effect of chronic insulin treatment in the osmotic shock signaling pathway leading to glucose uptake and GLUT-4 translocation.
Methods: 3T3-L1 adipocytcs were treated with 10 nM insulin for 10 hr and then acutely stimulated with 600 mM sorbitol or 16.6 nM insulin. We measured glucose transport and GLUT-4 translocation. We further determined Gab-1 phosphorylation Gab-1 associated PI 3-kinase activity and membrane ruffling.
Results: We found that chronic administration of insulin to the adipocytes induced cellular resistance to osmotic shock-stimulated glucose transport and GLUT-4 translocation. Chronic insulin treatment attenuated shock-induced Gab-1 tyrosine phosphorylation. Furthermore, chronic insulin exposure led to a marked impairment in the ability of Gab-1 to associate with p85 subunit of PI 3-kinase in response to acute shock and insulin stimulation. Cells that were chronically treated with insulin showed a 70% and an 85% decrease in Gab-1 associated PI 3-kinase activity in shock versus insulin treated cells, respectively. In addition, we found that chronic insulin treatment inhibited both insulin and osmotic shock-induced membrane ruffling, indicating that two PI 3-kinase dependent effects, GLUT-4 translocation and membrane ruffling are decreased in chronically insulin-treated cells.
Conclusions: The studies described above clearly demonstrate that chronic insulin exposure leads to desensitization of osmotic shock stimulated pathway and induces a state of cellular osmotic shock resistance for glucose transport and GLUT-4 translocation. It is possible that these findings may underlie the effect of insulin resistance on other insulinomimetic agents regulated pathways leading to GLUT-4 translocation and glucose transport.
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