Supplementing monosodium glutamate to partial enteral nutrition slows gastric emptying in preterm pigs(1-3)

Abstract

Emerging evidence suggests that free glutamate may play a functional role in modulating gastroduodenal motor function. We hypothesized that supplementing monosodium glutamate (MSG) to partial enteral nutrition stimulates gastric emptying in preterm pigs. Ten-day-old preterm, parenterally fed pigs received partial enteral nutrition (25%) as milk-based formula supplemented with MSG at 0, 1.7, 3.0, and 4.3 times the basal protein-bound glutamate intake (468 mg·kg(-1)·d(-1)) from d 4 to 8 of life (n = 5-8). Whole-body respiratory calorimetry and (13)C-octanoic acid breath tests were performed on d 4, 6, and 8. Body weight gain, stomach and intestinal weights, and arterial plasma glutamate and glutamine concentrations were not different among the MSG groups. Arterial plasma glutamate concentrations were significantly higher at birth than after 8 d of partial enteral nutrition. Also at d 8, the significant portal-arterial concentration difference in plasma glutamate was substantial (∼500 μmol/L) among all treatment groups, suggesting that there was substantial net intestinal glutamate absorption in preterm pigs. MSG supplementation dose-dependently increased gastric emptying time and decreased breath (13)CO2 enrichments, (13)CO2 production, percentage of (13)CO2 recovery/h, and cumulative percentage recovery of (13)C-octanoic acid. Circulating glucagon-like peptide-2 (GLP-2) concentration was significantly increased by MSG but was not associated with an increase in intestinal mucosal growth. In contrast to our hypothesis, our results suggest that adding MSG to partial enteral nutrition slows the gastric emptying rate, which may be associated with an inhibitory effect of increased circulating GLP-2.

FIGURE 1

Plasma free glutamate (A), glutamine (B), arginine (C), and aspartate (D) concentrations in arterial (d 0 and 8) and portal blood (d 8) of partially enterally fed preterm pigs receiving a milk-based formula (Control) or formula supplemented with various amounts of MSG. Values are means ± SEMs; n = 36 (d 0) or 5–8 (d 8). *P < 0.05, **P < 0.01, ***P < 0.001 vs. d 0, ^#P < 0.05, ^##P < 0.01, ^###P < 0.001 vs. arterial blood. MSG, monosodium glutamate.

FIGURE 2

Breath ¹³CO₂ enrichments (A), ¹³CO₂ production (B), % of ¹³CO₂ recovery/h (C), and cumulative percentage recovery of ¹³C-octanoic acid (D) determined at d 8 in partially enterally fed preterm pigs receiving a milk-based formula (Control) or formula supplemented with various amounts of MSG. Values are means ± SEMs; n = 5–7. APE, atom percent excess; MSG, monosodium glutamate.

FIGURE 3

T_1/2 (A) and T_lag (B) at d 8 in partially enterally fed preterm pigs receiving a milk-based formula (Control) or formula supplemented with various amounts of MSG and effect of time on T_lag and T_1/2 among all dietary treatment groups (C). Values are means ± SEMs; n = 5–7. MSG, monosodium glutamate; T_1/2, gastric half-emptying time; T_lag, gastric lag phase.

FIGURE 4

Arterial plasma GLP-2 concentrations determined at d 8 in partially enterally fed preterm pigs receiving a milk-based formula (Control) or formula supplemented with various amounts of MSG. Values are means ± SEMs; n = 6–8. Labeled means without a common letter differ, P < 0.05. GLP-2, glucagon-like peptide-2; MSG, monosodium glutamate.