Title: Supplementing monosodium glutamate to partial enteral nutrition slows gastric emptying in preterm pigs Authors
|Bauchart-Thevret, Caroline -|
|Stoll, Barbara -|
|Benight, Nancy -|
|Olutoye, Oluyinka -|
|Lazar, David -|
Submitted to: Journal of Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: March 13, 2012
Publication Date: February 27, 2013
Citation: Bauchart-Thevret, C., Stoll, B., Benight, N.M., Olutoye, O., Lazar, D., Burrin, D.G. 2013. Supplementing monosodium glutamate to partial enteral nutrition slows gastric emptying in preterm pigs. Journal of Nutrition. 143(5):563-570. Interpretive Summary: Glutamate is an important metabolic fuel source for intestinal cells. Glutamate also functions as a neurotransmitter in the body, and thus we hypothesized that dietary glutamate may influence digestive functions controlled by nerves in the gut. We tested this idea in premature piglets as a model for premature human infants. Premature human infants have feeding problems at birth that delay the rate of stomach digestion and prolong the time these infants need to remain in the hospital. We studied four groups of premature piglets fed a small amount of formula directly into the stomach for one week. We found that substantial amounts of dietary glutamate were absorbed into the bloodstream. We also found that adding free glutamate to the formula reduced the rate of stomach digestion and emptying. Added glutamate also increased the blood level of a gut hormone glucagon-like peptide 2, and this may be linked to the slower rate of stomach digestion. The finding suggests that the concentration of free glutamate in infant formulas may influence the rate of stomach digestion.
Technical 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 (of or about 500 micro mol per 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)CO enrichments, (13)CO production, percentage of (13)CO recovery per 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.