Rates of lactate appearance and disappearance and brain lactate balance after oral glucose in the dog.

Abstract

After glucose ingestion, arterial lactate concentrations increase. Although it is presumed that this is due to an increase in lactate production, rates of lactate appearance have not been measured after oral glucose nor has the major site of its production been identified. Since brain takes up a substantial portion of an oral glucose load but does not store appreciable amounts of glucose, it is possible that brain could be an important site for postprandial lactate formation. Therefore, to investigate the contribution of the brain to the increase in arterial lactate after glucose ingestion and to determine whether changes in lactate appearance or disappearance were predominantly involved, we measured lactate fluxes and brain lactate balance in dogs after intraduodenal administration of glucose (1.6 g/kg). Although systemic lactate appearance increased significantly after glucose administration (from 22 +/- 3 to 33 +/- 9 umole/kg/min, P less than 0.05), brain lactate output did not change (0.62 +/- 0.5 vs 0.74 +/- 0.5 umole/min). We conclude that after glucose ingestion, arterial lactate increases as a result of an increase in the rate of lactate appearance and that brain does not make a significant contribution to this.