Oxidation of glutamic acid by the splanchnic bed in humans.

[1,2-13C2]glutamate and [ring-2H5]phenylalanine were infused for 7 h into postabsorptive healthy subjects on two occasions. The tracer infusion was by the intravenous route for 3.5 h and by the nasogastric route for 3.5 h. The order of tracer infusion routes was switched between the two occasions. From the plasma tracer enrichment measurements at plateau during the intravenous and enteral infusion periods, we determined that 33 +/- 3% of the enterally delivered phenylalanine and 96 +/- 1% of the glutamate were removed on the first pass by the splanchnic bed; 78 +/- 3% of the enterally delivered [13C]glutamate tracer was recovered as exhaled CO2 compared with 79 +/- 2% of the intravenously infused tracer. The fraction of the enterally delivered tracer that was sequestered specifically on the first pass by the splanchnic bed was 75 +/- 2%. These results verify the previously reported large uptake of [15N]glutamate by the splanchnic bed [Matthews et al. Am. J. Physiol. 264 (Endocrinol. Metab. 27): E848-E854, 1993] and demonstrate that the uptake of tracer is not due to an artifactual loss of the 15N tracer by reversible transamination but to glutamate uptake for oxidation.