Fructose uptake in rat adipocytes: GLUT5 expression and the effects of streptozotocin-induced diabetes.
Previous studies have shown that rat adipocytes possess the capacity to take up fructose by a mechanism that is distinct from that involved in the transport of glucose. In this investigation we report that rat adipocytes express the GLUT5 fructose transporter and that it is responsible for mediating a substantial component (approximately 80%) of the total cellular fructose uptake. This proposition is based on the finding that only 21% of the total fructose uptake was cytochalasin B (CB) sensitive which most likely reflects transport via GLUT1 and/or GLUT4. Consistent with this suggestion we found (i) that insulin caused a small, but significant stimulation in fructose uptake (approximately 35%) which was abolished in the presence of CB and (ii) that 3-O-methyl glucose inhibited fructose uptake to a level comparable with that observed in the presence of CB. GLUT5 was found to be localised only in the adipocyte plasma membrane and, unlike GLUT4 or GLUT1, its cell surface abundance was not modulated by insulin. GLUT5 expression fell substantially (by approximately 75%) in adipocytes of streptozotocin-diabetic rats and was accompanied by a reduction in fructose uptake by approximately 50%. Treatment of streptozotocin-diabetic rats with sodium orthovanadate for a period of 3 days led to a significant reduction in blood glycaemia by approximately 40% and a partial restoration in both GLUT5 expression and adipocyte fructose uptake. We suggest that fructose uptake in rat adipocytes is principally mediated by GLUT5 in an insulin- and CB-insensitive manner and that expression of GLUT5 in rat adipocytes may be regulated by changes in blood glycaemia.
Department of Anatomy and Physiology, The University of Dundee, Scotland, UK.
E
E
Hajduch
F
F
Darakhshan
H S
HS
Hundal
D019325:3-O-Methylglucose / Q000494:pharmacology; D017667:Adipocytes / Q000187:drug effects / Q000378:metabolism*; D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D002462:Cell Membrane / Q000378:metabolism; D002478:Cells, Cultured; D003571:Cytochalasin B / Q000494:pharmacology; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000378:metabolism*; D004822:Epididymis; D005632:Fructose / Q000378:metabolism*; D005786:Gene Expression Regulation; D051272:Glucose Transporter Type 1; D051275:Glucose Transporter Type 4; D051296:Glucose Transporter Type 5; D007328:Insulin / Q000494:pharmacology* / Q000502:physiology; D007700:Kinetics; D008297:Male; D009004:Monosaccharide Transport Proteins / Q000096:biosynthesis* / Q000235:genetics / Q000378:metabolism; D009124:Muscle Proteins; D051381:Rats; D017207:Rats, Sprague-Dawley; D014638:Vanadates / Q000494:pharmacology
D001786:Blood Glucose; D051272:Glucose Transporter Type 1; D051275:Glucose Transporter Type 4; D051296:Glucose Transporter Type 5; D007328:Insulin; D009004:Monosaccharide Transport Proteins; D009124:Muscle Proteins; C495679:Slc2a1 protein, rat; C495694:Slc2a4 protein, rat; D019325:3-O-Methylglucose; D005632:Fructose; D003571:Cytochalasin B; D014638:Vanadates