FRUCTOSE UPTAKE IN RAT ADIPOCYTES - GLUT5 EXPRESSION AND THE EFFECTS OF STREPTOZOTOCIN-INDUCED DIABETES

Previous studies have shown that rat adipocytes possess the capacity t o 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 GLUTS fructose transporter and that it is respo nsible for mediating a substantial component (similar to 80%) of the t otal cellular fructose uptake. This proposition is based on the findin g 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 sm all, but significant stimulation in fructose uptake (similar to 35 %) which was abolished in the presence of CB and (ii) that 3-O-methyl glu cose inhibited fructose uptake to a level comparable with that observe d in the presence of CB. GLUTS was found to be localised only in the a dipocyte plasma membrane and, unlike GLUT4 or GLUT1, its cell surface abundance was not modulated by insulin. GLUTS expression fell substant ially (by similar to 75 %) in adipocytes of streptozotocin-diabetic ra ts and was accompanied by a reduction in fructose uptake by approximat ely 50%. Treatment of streptozotocin-diabetic rats with sodium orthova nadate for a period of 3 days led to a significant reduction in blood glycaemia by approximately 40% and a partial restoration in both GLUTS expression and adipocyte fructose uptake. We suggest that fructose up take in rat adipocytes is principally mediated by GLUTS in an insulin- and CB-insensitive manner and that expression of GLUTS in rat adipocy tes may be regulated by changes in blood glycaemia.