Previous studies indicating that postabsorptive renal glucose production is negligible used the net balance technique, which cannot partition simultaneous renal glucose production and glucose uptake. 10 d after surgical placement of sampling catheters in the left renal vein and femoral artery and a nonobstructive infusion catheter in the left renal artery of dogs, systemic and renal glucose and glycerol kinetics were measured with peripheral infusions of [3-3H]glucose and [2-14C]glycerol. After baseline measurements, animals received a 2-h intrarenal infusion of either insulin (n = 6) or saline (n = 6). Left renal vein insulin concentration increased from 41±8 to 92±23 pmol/l (P < 0.05) in the insulin group, but there was no change in either arterial insulin, (~ 50 pmol/l), glucose concentrations (~ 5.4 mmol/l), or glucose appearance (~ 18 μmol · kg-1 · min-1). Left renal glucose uptake increased from 3.1±0.4 to 5.4±1.4 μmol · kg-1 · min-1 (P < 0.01) while left renal glucose production decreased from 2.6±0.9 to 0.7±0.5 μmol · kg-1 · min-1 (P < 0.01) during insulin infusion. Renal gluconeogenesis from glycerol decreased from 0.23±0.06 to 0.17±0.04 μmol · kg-1 · min-1 (P < 0.05) during insulin infusion. These results indicate that renal glucose production and utilization account for ~ 30% of glucose turnover in postabsorptive dogs. Physiological hyperinsulinemia suppresses renal glucose production and stimulates renal glucose uptake by ~ 75%. We conclude that the kidney makes a major contribution to systemic glucose metabolism in the postabsorptive state.
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