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Am J Physiol Endocrinol Metab 269: E897-E902, 1995;
0193-1849/95 $5.00
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AJP - Endocrinology and Metabolism, Vol 269, Issue 5 E897-E902, Copyright © 1995 by American Physiological Society


ARTICLES

Human GLUT-2 overexpression does not affect glucose-stimulated insulin secretion in MIN6 cells

H. Ishihara, T. Asano, K. Tsukuda, H. Katagiri, K. Inukai, M. Anai, Y. Yazaki, J. Miyazaki, M. Kikuchi and Y. Oka
Institute for Adult Diseases, Asahi Life Foundation, Tokyo, Japan.

Accumulated evidence suggests that GLUT-2, in addition to its role in glucose transport, may also have other functions in glucose-stimulated insulin secretion. As a first step in addressing this possibility, we have engineered MIN6 cells overexpressing human GLUT-2 by transfection with human GLUT-2 cDNA. Stable transformants harboring human GLUT-2 cDNA exhibited an approximately twofold increase in 3-O-methyl-D-glucose uptake at 0.5 and 15 mM. Glucokinase activity or glucose utilization measured by conversion of [5-3H]glucose to [3H]H2O was not, however, altered in the MIN6 cells overexpressing human GLUT-2. Furthermore, glucose-stimulated insulin secretion was not affected by over-expression of human GLUT-2. An abundance of GLUT-2, therefore, does not correlate with the glucose responsiveness of cells in which glycolysis is regulated at the glucose phosphorylating step. These data suggest that GLUT-2 by itself does not have significant functions other than its role in glucose transport in glucose sensing by MIN6 cells.





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