Translocation of the brain-type glucose transporter largely accounts for insulin stimulation of glucose transport in BC3H-1 myocytes.
Insulin-stimulated glucose transport was examined in BC3H-1 myocytes. Insulin treatment lead to a 2.7 +/- 0.3-fold increase in the rate of deoxyglucose transport and, under the same conditions, a 2.1 +/- 0.1-fold increase in the amount of the brain-type glucose transporter (GLUT 1) at the cell surface. It has been shown that some insulin-responsive tissues express a second, immunologically distinct, transporter, namely GLUT 4. We report here that BC3H-1 myocytes and C2 and G8 myotubes express only GLUT 1; in contrast, rat soleus muscle and heart express 3-4 times higher levels of GLUT 4 than GLUT 1. Thus translocation of GLUT 1 can account for most, if not all, of the insulin stimulation of glucose transport in BC3H-1 myocytes. On the other, hand, neither BC3H-1 myocytes nor the other muscle-cell lines are adequate as models for the study of insulin regulation of glucose transport in muscle tissue.
Department of Biochemistry, Dartmouth Medical School, Hanover, NH 03756.
D M
DM
Calderhead
K
K
Kitagawa
G E
GE
Lienhard
G W
GW
Gould
D000818:Animals; D001923:Brain Chemistry; D002460:Cell Line; D002462:Cell Membrane / Q000648:ultrastructure; D007328:Insulin / Q000494:pharmacology*; D051379:Mice; D009004:Monosaccharide Transport Proteins / Q000493:pharmacokinetics*; D009132:Muscles / Q000032:analysis / Q000166:cytology / Q000378:metabolism*; D013268:Stimulation, Chemical
D007328:Insulin; D009004:Monosaccharide Transport Proteins