The goal of the project is to describe the mechanisms involved in the regulation of carrier-mediated sugar transport in heart muscle and avian erythrocytes. In our earlier studies, sugar transport in these cells was found to be a passive process involving a mobile carrier. Transport is accelerated in avian erythrocytes by anoxia, sulfhydryl- blocking agents, epinephrine and addition of ATP to the incubation medium. In heart muscle, anoxia, insulin, the level of ventricular pressure development, and the availability of fatty substrates modify transport rate. We propose to investigate 1) the effects of anoxia, ventricular pressure development, and insulin on the kinetics of glucose transport in heart muscle; 2) the effects of anoxia, sulfhydryl-blocking agents, and epinephrine on the kinetics of non-metabolized sugar transport in avian erythrocytes; 3) the effects of potential regulators of transport on rates of entry and exit of sugar from reversibly-hemolyzed erythrocytes and 4) the relationship of phosphorylation of membrane components to regulation of transport rate. These studies will allow for test of models of transport regulation involving 1) changes in the level of membrane phosphorylation or 2) changes in the levels of intracellular compounds that modulate carrier activity. Bibliographic references: Whitfield, C.F. Erythrocyte membrane phosphorylation and sugar transport. Fed. Proc. 34:237, 1975; Whitfield, C.F., Rannels, S.R. and Morgan, H.E. Acceleration of sugar transport in avian erythrocytes by catecholamines. J. Biol. Chem. 249:4181-4188, 1974.
NIH ExPorter
NIH ExPorter