Monosodium glutamate raises antral distension and plasma amino acid after a standard meal in humans

Abstract

The consumption of monosodium glutamate (MSG) is advocated to elicit physiological and metabolic effects, yet these effects have been poorly investigated directly in humans and in particular in the postprandial phase. Thirteen healthy adults were supplemented for 6 days with a nutritional dose of MSG (2 g) or sodium chloride (NaCl) as control, following a crossover design. On the 7th day, they underwent a complete postprandial examination for the 6 h following the ingestion of the same liquid standard meal (700 kcal, 20% of energy as [(15)N]protein, 50% as carbohydrate, and 30% as fat) supplemented with MSG or NaCl. Real-ultrasound measures of antral area indicated a significant increased distension for the 2 h following the meal supplemented with MSG vs. NaCl. This early postprandial phase was also associated with significantly increased levels of circulating leucine, isoleucine, valine, lysine, cysteine, alanine, tyrosine, and tryptophan after MSG compared with NaCl. No changes to the postprandial glucose, insulin, glucagon-like peptide (GLP)-1, and ghrelin were noted between MSG- and NaCl-supplemented meals. Subjective assessments of hunger and fullness were neither affected by MSG supplementation. Finally, the postprandial fate of dietary N was identical between dietary conditions. Our findings indicate that nutritional dose of MSG promoted greater postprandial elevations of several indispensable amino acids in plasma and induced gastric distension. Further work to elucidate the possible sparing effect of MSG on indispensable amino acid first-pass uptake in humans is warranted. This trial was registered at clinicaltrials.gov as NCT00862017.

Correlation Between Gastric Emptying and Gastric Adaptive Relaxation Influenced by Amino Acids

“…18 In a dog model, aspartic acid did not influence gastric emptying, 4 but in this study it inhibited and delayed gastric emptying. Food intake was most potently reduced by oral Lglutamic acid in rats, 5 and also in a clinical study, monosodium glutamate increased antral distension, 23 supporting our present results. However, these conflicting results may be due to the differences in experimental conditions.…”

Umami Receptor Activation Increases Duodenal Bicarbonate Secretion via Glucagon-Like Peptide-2 Release in Rats

“…Artificial sweeteners, which serve as high-affinity T1R2/R3 ligands, fail to release GLP-1 in rats in vivo, in humans, and from purified L cells (Reimann et al, 2008;Fujita et al, 2009;Little et al, 2009;Ma et al, 2009), demonstrating that glucose sensing in L cells is not likely mediated by T1R2/R3. Furthermore, L-Glu meal supplementation had no effect on circulating postprandial plasma concentrations of glucose, insulin, glucagon, or GLP-1 in humans (Boutry et al, 2011). Although glucose-induced GLP-1 release is probably mediated by the sodium-glucose cotransporter SGLT1 in L cells, rather than by the T1R2/R3 sweet receptor, our finding that luminal L-Glu/IMP releases GLP-2 via T1R1/R3 activation remains possible.…”

Monosodium Glutamate Toxic Effects and Their Implications for Human Intake: A Review

“…MSG intake was also associated with increased levels of some circulating amino acids (leucine, isoleucine, valine, lysine, cysteine, alanine, tyrosine, and tryptophan) compared with controls. No changes in the postprandial glucose and insulin were noted between MSG and NaClsupplemented meals used in controls (Boutry et al 2011), which is a significant difference _______________ Veronika Daniela Ostatnikova (2013), JMED Research, DOI: 10.5171/2013.608765 from previously mentioned animal studies. However the insulin response in 75 min postprandially positively correlated with the plasma glutamate concentration during the oral glucose tolerance test, which indicates that glutamate can participate in the insulin response to nutrients during food intake (Chevassus et al 2002).…”