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/10(6) 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 Vmax of the transporter system: Vmax = 5.9 +/- 0.8 and 12.1 +/- 1.2 fmol/10(6) cells/min for lean and obese cells, respectively (P < .05); no changes in Km were noted for the two populations: Km = 1.14 +/- 0.24 and 0.96 +/- 0.10 mmol/L. Insulin (10 microU/mL) increased the Vmax 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 Km 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.