Increased basal arterial smooth muscle glucose transport in the Zucker rat

Insulin has recently been reported to stimulate glucose transport in vascular smooth muscle cells (VSMC). This observation suggests a role for this hormone in hypertension associated with insulin resistance. To determine whether VSMC glucose transport abnormalities exist in a state of insulin resistance, we studied basal and insulin-stimulated glucose transport in VSMC derived from Zucker lean (normotensive, insulin sensitive) and obese (hypertensive, insulin resistant) rats. Basal glucose transport, as measured by tracer quantities of [³H]2-deoxyglucose, was 4.2 ± 0.8 and 7.4 ± 0.9 fmol/10⁶ cells/min for lean and obese cells, respectively (P < .05). Kinetic analyses utilizing variable concentrations of unlabeled 2-deoxyglucose in the media revealed that increased transport in the obese rat was due to an increased V_max of the transporter system: V_max = 5.9 ± 0.8 and 12.1 ± 1.2 fmol/10⁶ cells/min for lean and obese cells, respectively (P < .05); no changes in K_m were noted for the two populations: K_m 1.14 ± 0.24 and 0.96 ± 0.10 mmol/L. Insulin (10 μU/mL) increased the V_max of the transporter in both preparations, but greater stimulation was seen in the lean VSMC: 32 ± 4.8% v 11.5 ± 2.1% (P < .05). Insulin had no effect on the K_m of the transporter in either strain. These data suggest that increased basal glucose transport in obese VSMC may predispose the vessel to increased glucose-mediated events, while blunted insulin-stimulated glucose transport in these cells mirrors insulin-resistant glucose disposal in other tissues of the obese rat.