AENDO April 41/4

Haisch, M., N. K. Fukagawa, and D. E. Matthews. Oxidation of glutamine by the splanchnic bed in humans. Am J Physiol Endocrinol Metab 278: E593–E602, 2000.—[1,2C2]glutamine and [ring-H5]phenylalanine were infused for 7 h into five postabsorptive healthy subjects on two occasions. On one occasion, the tracers were infused intravenously for 3.5 h and then by a nasogastric tube for 3.5 h. The order of infusion was reversed on the other occasion. From the plasma tracer enrichment measurements at plateau during the intravenous and nasogastric infusion periods, we determined that 27 6 2% of the enterally delivered phenylalanine and 64 6 2% of the glutamine were removed on the first pass by the splanchnic bed. Glutamine flux was 303 6 8 μmol ·kg21 ·h21. Of the enterally delivered [13C]glutamine tracer, 73 6 2% was recovered as exhaled CO2 compared with 58 6 1% of the intravenously infused tracer. The fraction of the enterally delivered tracer that was oxidized specifically on the first pass by the splanchnic bed was 53 6 2%, comprising 83% of the total tracer extracted. From the appearance of 13C in plasma glucose, we estimated that 7 and 10% of the intravenously and nasogastrically infused glutamine tracers, respectively, were converted to glucose. The results for glutamine flux and first-pass extraction were similar to our previously reported values when a [2-15N]glutamine tracer [Matthews DE, Morano MA, and Campbell RG, Am J Physiol Endocrinol Metab 264: E848–E854, 1993] was used. The results of [13C]glutamine tracer disposal demonstrate that the major fate of enteral glutamine extraction is for oxidation and that only a minor portion is used for gluconeogenesis.