Potentiation of 14C-glucose oxidation by priming glucose loads: effect of starvation

The mechanism of the Staub-Traugott effect or facilitated glucose disposal after successive glucose loads has remained elusive. In earlier publications, we have shown it can be independent of circulating hormone and free fatty acid levels. We have also proposed that it might partially depend on the rapid induction of glycolytic pathways, which are known to be depressed by prolonged fast. Mature rats were given 1.75 gm/kg glucose doses intravenously at 60-minute intervals. Respiratory CO2 was collected at 15-minute intervals over a 120-minute period following administration of the carrier glucose plus 6 microCi/100 gm rat weight of 14C-D-glucose, given either as the first, second, or third challenge. In rats fasted 14 hours there was potentiation of labeled CO2 recovered after each successive load. After three days of starvation, both relative 14C-glucose oxidation to 14CO2 as well as absolute 14CO2 increments after each load were lower. The changes in relative oxidation of an intravenous glucose load might partly account for the facilitated disposal of blood glucose seen in the second and third hours in overnight-fasted rats (Staub-Traugott effect). However, although rats fasted for three days had suppressed the Staub effect, the increments in oxidation were attenuated but still present, suggesting that alterations of other pathways must participate in the disappearance of this effect after fasting.