Cytokine Stimulation Promotes Increased Glucose Uptake Via Translocation at the Plasma Membrane of GLUT1 in HEK293 Cells

Zambrano, A; Jara, E; Murgas, P; Jara, C; Castro MA; Angulo, C; Concha, II

Abstract

Interleukin-3 (IL-3) and granulocyte/macrophage colony-stimulating factor (GM-CSF) are two of the best-characterized cell survival factors in hematopoietic cells; these factors induce an increase in Akt activity in multiple cell lines, a process thought to be involved in cellular survival. It is known that growth factors require sustained glucose metabolism to promote cell survival. It has been determined that IL-3 and GM-CSF signal for increased glucose uptake in hematopoietic cells. Interestingly, receptors for IL-3 and GM-CSF are present in several nonhematopoietic cell types but their roles in these cells have been poorly described. In this study, we demonstrated the expression of IL-3 and GM-CSF receptors in HEK293 cells and analyzed their effect on glucose uptake. In these cells, both IL-3 and GM-CSF, increased glucose uptake. The results indicated that this increase involves the subcellular redistribution of GLUT1, affecting glucose transporter levels at the cell surface in HEK293 cells. Also the data directly demonstrates that the PI 3-kinase/Akt pathway is an important mediator of this process. Altogether these results show a role for non-insulin growth factors in the regulation of GLUT1 trafficking that has not yet been directly determined in non-hematopoietic cells. © 2010 Wiley-Liss, Inc.

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Título según WOS: Cytokine Stimulation Promotes Increased Glucose Uptake Via Translocation at the Plasma Membrane of GLUT1 in HEK293 Cells
Título según SCOPUS: Cytokine stimulation promotes increased glucose uptake via translocation at the plasma membrane of GLUT1 in HEK293 cells
Título de la Revista: JOURNAL OF CELLULAR BIOCHEMISTRY
Volumen: 110
Número: 6
Editorial: WILEY-BLACKWELL
Fecha de publicación: 2010
Página de inicio: 1471
Página final: 1480
Idioma: English
URL: http://doi.wiley.com/10.1002/jcb.22711
DOI:

10.1002/jcb.22711

Notas: ISI, SCOPUS