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GLUT4 glucose transporter

Individuals with either type of diabetes are unable to take up glucose efficiently from the blood recall that insulin triggers the movement of GLUT4 glucose transporters to the plasma membrane of muscle and adipose tissue (see Fig. 12-8). Another characteristic metabolic change in diabetes is excessive but incomplete oxidation of fatty acids in the liver. The acetyl-CoA produced by JS oxidation cannot be completely oxidized by the citric acid cycle, because the high [NADH]/[NAD+] ratio produced by JS oxidation inhibits the cycle (recall that three steps convert NAD+ to NADH). Accumulation of acetyl-CoA leads to overproduction of the ketone bodies acetoacetate and /3-hydroxybutyrate, which cannot be used by extrahepatic tissues as fast as they are made in the liver. In addition to /3-hydroxybutyrate and acetoacetate, the blood of diabetics also contains acetone, which results from the spontaneous decarboxylation of acetoacetate ... [Pg.909]

Weinstein, S. P., Holand, A., O Boyle, E., and Haber, R. S. (1993). Effects of Thia-zolidinediones on Glucocorticoid-Induced Insulin Resistance and GLUT4 Glucose Transporter Expression in Rat Skeletal Muscle. Metabolism 42, 1365-1369. [Pg.208]

Hansen, R, Gulve, E., Marshall, B., Gao, J. Pessin, J., HoUoszy, J., and Mueckler, M. (1995). Skeletal muscle glucose transport and metabolism are enhanced in transgenic mice overexpressing the glut4 glucose transporter. J. Biol. Chem. 270,1679-1684. [Pg.129]

Holman, G.D., Lo Leggio, L., Cushman, S.W. 1994. Insulin-stimulated GLUT4 glucose transporter recycling. A problem in membrane protein subcellular trafficking through multiple pools. J. Biol. Chem. 269 17516-17524. [Pg.304]

ABBREVIATIONS APS, adaptor protein with PH and SH2 domains CAP, Cbl associated protein Crkll, chicken tumor virus regulator of kinase II GLUT4, glucose transporter 4 Gab-1, Grb-2 associated binder MAP kinase, mitogen-activated protein kinase PDK, phosphoinositide-dependent kinase PI3 kinase, phosphatidylinositol-3-kinase PIP3, phos-phatidylinositol trisphosphate PKB, protein kinase B (also called Akt) aPKC, atypical isoform of protein kinase C Y, tyrosine residue Y-P, phosphorylated tyrosine residue. [Pg.1039]

AKT was previously known as PKB. Insulin has scores of different effects on cells. It can stimulate the translocation of GLUT4 glucose transporters to the plasma membrane, and stimulate fatty add synthesis, protein synthesis, glycogen synthesis, etc. Remarkably, aU these... [Pg.63]


See other pages where GLUT4 glucose transporter is mentioned: [Pg.463]    [Pg.357]    [Pg.580]    [Pg.170]    [Pg.120]    [Pg.121]    [Pg.201]    [Pg.141]    [Pg.23]    [Pg.129]    [Pg.2418]    [Pg.69]    [Pg.110]    [Pg.174]    [Pg.600]    [Pg.618]    [Pg.1039]    [Pg.149]    [Pg.296]    [Pg.63]    [Pg.4144]    [Pg.553]   
See also in sourсe #XX -- [ Pg.121 ]




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