TAILIEUCHUNG - Báo cáo khoa học: Arsenite stimulated glucose transport in 3T3-L1 adipocytes involves both Glut4 translocation and p38 MAPK activity

The protein-modifying agent arsenite stimulates glucose uptake in 3T3-L1 adipocytes. In the current study we have analysed the signalling pathways that contribute to this response. By subcellular fractionation we observed that arsenite, like insulin, induces translocation of the GLUT1 and GLUT4 glucose transporters from the low-density membrane fraction to the plasma membrane. Arsenite did not activate early steps of the insulin receptor (IR)-signalling pathway and the response was insensitive to inhibition of phosphatidylinositol-3¢-kinase (PI-3¢)kinaseby wortman-nin. . | Eur. J. Biochem. 270 3891-3903 2003 FEBS 2003 doi Arsenite stimulated glucose transport in 3T3-L1 adipocytes involves both Glut4 translocation and p38 MAPK activity Merlijn Bazuine D. Margriet Ouwens Daan S. Gomes de Mesquita and J. Antonie Maassen Department of Molecular Cell Biology Leiden University Medical Centre Leiden the Netherlands The protein-modifying agent arsenite stimulates glucose uptake in 3T3-L1 adipocytes. In the current study we have analysed the signalling pathways that contribute to this response. By subcellular fractionation we observed that arsenite like insulin induces translocation of the GLUT1 and GLUT4 glucose transporters from the low-density membrane fraction to the plasma membrane. Arsenite did not activate early steps of the insulin receptor IR -signalling pathway and the response was insensitive to inhibition of phosphatidylinositol-3 -kinase PI-3 kinase by wortman-nin. These findings indicate that the classical IR-IR substrate-PI-3 kinase pathway that is essential for insulin-induced GLUT4 translocation is not activated by arsenite. However arsenite-treatment did induce tyrosinephosphorylation of c-Cbl. Furthermore treatment of the cells with the tyrosine kinase inhibitor tyrphostin A25 abolished arsenite-induced glucose uptake suggesting that the induction of a tyrosine kinase by arsenite is essential for glucose uptake. Both arsenite and insulin-induced glucose uptake were inhibited partially by the p38 MAP kinase inhibitor SB203580. This compound had no effect on the magnitude of translocation of glucose transporters indicating that the level of glucose transport is determined by additional factors. Arsenite- and insulin-induced glucose uptake responded in a remarkably similar dose-dependent fashion to a range of pharmacological- and peptide-inhibi-tors for atypical PKC-k a downstream target of PI-3 kinase signalling in insulin-induced glucose uptake. These data show that in 3T3-L1 adipocytes both

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