EFFECT OF A MIXED MEAL ON HEPATIC LACTATE AND GLUCONEOGENIC PRECURSOR METABOLISM IN DOGS

The present experiments were undertaken to assess lactate and gluconeogenic precursor metabolism in the 30 h following consumption of a mixed meal by the overnight-fasted, conscious dog. The arterial glucose level rose by a maximum of 13 mg/dl 4 h after the meal and had returned to control levels by 12 h. Hepatic glucose production was suppressed for 12 h after feeding, but net hepatic glucose uptake did not occur. The arterial lactate level rose from 0.55 .+-. 0.10 to 1.28 .+-. 0.14 mM within 1 h of feeding and remained elevated for 12 h. Net hepatic lactate production, measured with an arteriovenous difference technique, rose from 3.5 .+-. 2.8 to 19.4 .+-. 3.1 .mu.mol/kg per min 1 h after the meal and declined slowly over the next 22 h. The liver then began to consume lactate so that at 30 h net hepatic uptake was 5.7 .+-. 0.5 .mu.mol/kg per min. The total hepatic uptake of the gluconeogenic amino acids (Ala, Gly, Ser, Thr) increased from 5.3 .+-. 0.8 to 11.5 .+-. 2.5 .mu.mol/kg per min at 1 h and remained elevated for 18 h. Insulin increased from 11 .+-. 2 .mu.U/ml to a maximum of 44 .+-. 5, 4 h after the meal, and the glucagon level rose from 59 .+-. 8 pg/ml to a maximum of 150 .+-. 22 1 h after feeding. The plasma concentrations of both hormones had returned to control levels by 12 h. In a dog fed a mixed meal once every 24 h the postprandial hyperlactemia is of hepatic origin, the Cori cycle does not contribute any carbon for net glucose synthesis, and a significant amount of the net carbon required for postprandial hepatic glycogen synthesis must come from sources other than circulating lactate and glucose.