- 作者: Ying-Shun Kao; Jjm C. Fong
- 作者服務機構: Institute of Biochemistry, National Yang-Ming University, Taipei, Taiwan/ROC
- 中文摘要: --
- 英文摘要: We have previously demonstrated that ET-1 may en-hance glucose transport in 3T3-L1 adipocytes, secondari-ly to its stimulatory effect on GLUT1 gene expression bya mitogen-activated protein kinase(MAPK)-dependentpathway. In the present study, we further tested theinvolvement of Ca 2+ in glucose uptake in response toET-1 .Among a variety of Ca2-related agents tested,EGTA and thapsigargin were found to suppress both theglucose uptake and intracellular Ca2+ mobilization in-duced by ET-1,as determined by Fura-2 analysis. How-ever, a phospholipase C inhibitor, U73122, also elimi-nated the intracellular calcium mobilization induced byET-1,but had no effect on ET-1-stimulated glucose up-take.The finding that neither EGTA nor thapsigargin hadany influence on ET-1一induced MAPK activation impliesthat some mechanism downstream of MAPK activationis involved. Further investigation showed that bothagents exerted global inhibitory effects on protein andRNA syntheses. Since both thapsigargin and EGTA maydeplete endoplasmic reticulum(ER)Ca2+ stores, ourresuIts suggest that(1)ET-1-induced glucose transport isindependent of ET-1's effect on Ca2+ mobilization and(2)depletion of ER Ca2+ stores per se may interfere withET-1's effect on GLUT1 expression.
- 中文關鍵字: --
- 英文關鍵字: --