|Burrin, Douglas - Doug|
Submitted to: Pediatric Research
Publication Type: Peer reviewed journal
Publication Acceptance Date: 4/20/2007
Publication Date: 9/7/2007
Citation: Hays, S.P., Ordonez, J.M., Burrin, D.G., Sunehag, A.L. 2007. Dietary glutamate is almost entirely removed in its first pass through the splanchnic bed in premature infants. Pediatric Research. 62(3):353-356. Interpretive Summary: Glutamate, the most abundant amino acid in breast milk, is a potential substrate for the body’s sugar production. However, in piglets most dietary glutamate is taken up by the gut, limiting its contribution to sugar formation. The objectives of this study were to determine whether dietary glutamate appears in the blood in a dose-dependent fashion, and whether glutamate carbon appears in the blood sugar to an appreciable extent. Five enterally fed infants (31+/-0 wks; 1555+/-131 g) were studied twice at 10 and 17 days, respectively, after birth. On the first occasion they received glutamate corresponding to twice that of breast milk and on the second occasion four times that of breast milk via a feeding tube placed for clinical purposes. The glutamate was labeled with a stable, non-radioactive naturally occurring tracer. The results demonstrated that dietary glutamate does not appear in plasma in a dose-dependent fashion in premature infants. Further, the contribution from dietary glutamate to glucose formation is minimal in these infants. We also conclude that in premature infants the major part of dietary glutamate is taken up by the gut and that dietary glutamate is not an import substrate for the body’s sugar production.
Technical Abstract: 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 [glutamate] 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 +/- 1 d and 17 +/- 1 d, respectively), while receiving an intragastric infusion of glutamate (labeled to 4% by [U-C] glutamate) at 2.4 (study 1) and 4.8 mumol/kg/min (study 2) for 1.5 h (n = 2) or 5 h (n = 3). Plasma [glutamate] was 82 +/- 8 muM at baseline, and 84 +/- 11 and 90 +/- 13 muM after glutamate supplementation at 2.4 and 4.8 mumol/kg/min, 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 glucose enrichment was only 0.3% (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.