Dietary glutamate is almost entirely removed in its first pass through the splanchnic bed in premature infants

Breast milk glutamate is a potential gluconeogenic substrate. However, in piglets, most dietary glutamate undergoes first pass extraction by the gut, limiting its contribution to glucose formation. The objectives of the study were to determine in preterm infants, whether dietary glutamate increases plasma [glutannate] in a dose-dependent fashion and whether glutamate carbon appears in plasma glucose to an appreciable extent. Five enterally fed infants (31 +/- 0 wk: 1555 +/- 131 g) (mean - SE) were studied twice (postnatal age 10 +/- Id and 17 Id, respectively), while receiving an intrauastric infusion of glutamate (labeled to 4% by [U-C-13] glutamate) at 2.4 (study 1) and 4.8 mu mol/kg/min (study 2) for 1.5 h (n = 2) or 5 h (n = 3). Plasma [glutamate] was 82 +/- 8 AM at baseline, and 84 +/- 11 and 90 +/- 13 AM after glutamate supplementation at 2.4 and 4.8 mu mol/kg/lutin, respectively, values not different from baseline. Plasma [glutamate] was not affected by the duration of the glutamate infusion (1.5 versus 5 h). Plasma C-13 glucose enrichment was only 0.317% (after 5 h ingestion of glutamate labeled to 4%) indicating insignificant contribution of dietary glutamate carbon to glucose. Thus. in premature infants, splanchnic extraction is the major fate of dietary glutamate, which is not a significant gluconeogenic substrate in these infants.