Submitted to: Meeting Abstract
Publication Type: Abstract only
Publication Acceptance Date: 2/1/2006
Publication Date: 6/9/2006
Citation: Ordonez, J., Hays, S.P., Sunehag, A.L. 2006. In premature infants, dietary glutamate is almost entirely removed in its first pass through the splanchnic bed [abstract]. 2006 Pediatric Academic Societies Meeting. Paper No. 753345. Interpretive Summary:
Technical Abstract: Background: Glutamate is an important gluconeogenic substrate. Breast milk glutamate, its most abundant amino acid, may thus play an important role in glucose production. However, studies in infant pigs have demonstrated that the major portion of intragastrically administered glutamate undergoes first pass splanchnic extraction, limiting its contribution to new blood glucose carbon. Whether this is the case in human preterm infants is unknown. Objective: To determine in preterm infants whether intragastrically administered glutamate increases plasma glutamate concentration in a dose dependent fashion and, correspondingly, whether glutamate carbon appears in plasma glucose to an appreciable extent, secondary to gluconeogenesis. Design/Methods: Five premature infants (31+/- 0 wks; 1555+/-131 g) were studied on two occasions at a postnatal age of 10+/- 1 d (study 1) and 17+/- 1 d (study 2). All infants were fed enterally. The infants received a regular feeding followed by either a 1.5 (n=2) or 5 h (n=3) intragastric infusion of glutamate at 2.4 umol/kg min (study 1) and 4.8 umol/kg min (study 2). These rates correspond to two and four times, respectively, the glutamate provided by 4.5 ounces of breast milk/kg d. Four percent of the glutamate was [U-13C]glutamate. Blood samples were obtained before the feeding (baseline) and at the end of the glutamate ingestion. Results: Baseline glutamate concentration was 82+/-8 uM (mean SE); after a regular feeding + supplemental glutamate at 2.4 umol/kg min, plasma [glutamate] was 84+/- 11 uM and after a regular feeding + supplemental glutamate at 4.8 umol/kg min, plasma [glutamate] was 90+/- 13 uM. The data were analyzed by ANOVA followed by Fisher’s pairwise comparisons, demonstrating that intragastric supplementation of glutamate at either 2.4 umol/kg min or 4.8 umol/kg min did not increase plasma [glutamate] when compared to baseline. Likewise, the duration of the glutamate infusion (1.5 vs. 5 h) had no effect on plasma [glutamate]. Five hours after ingestion of glutamate labeled at the 4 percent level, Plasma [U-13C]glutamate enrichment was only ~0.26 percent, indicating minimal contribution of dietary glutamate carbon to blood glucose carbon. Conclusions: In premature infants, splanchnic extraction is the major fate of dietary glutamate. Dietary glutamate is not a significant gluconeogenic substrate in preterm infants.