Effect of carbohydrate on plasma and erythrocyte glutamate levels in humans ingesting large doses of monosodium L-glutamate in water

Stegink, Lewis D.; Filer, L. J.; Baker, George L.

doi:10.1093/ajcn/37.6.961

Cited by 41 publications

(44 citation statements)

References 29 publications

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“…When MSG (150 mg/kg bw) was given together with carbohydrate (1.1 g/kg bw in the form of hydrolyzed corn starch), time to reach the plasma glutamate peak and time to return to basal were similar to the values observed when glutamate was given alone [19]. However, the peak plasma concentration was lowered ( Table 2).…”

Section: Pharmacokinetics Of Dietary Glutamatesupporting

confidence: 54%

“…There was no change in glutamate levels in red blood cells [19]. Some years later, Graham et al [24] conducted a similar study and obtained closely similar results.…”

Section: Pharmacokinetics Of Dietary Glutamatementioning

confidence: 66%

“…Stegink et al [19] conducted an impressive series of studies in which glutamate (as monosodium salt) was administered alone, with carbohydrate [19,20], with a con- somme [20,21] or with meals [22,23]. The results of these studies are summarized in Table 2.…”

Section: Pharmacokinetics Of Dietary Glutamatementioning

confidence: 99%

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Metabolism of Dietary Glutamate in Adults

Cynober

2018

Ann Nutr Metab

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Background: Glutamate is a non-essential amino acid at the crossroads of nitrogen and energy metabolism. Glutamate metabolism is characterized by reactions that may be anabolic or catabolic in nature depending on the tissue (i.e., glutamate dehydrogenase, transaminases), and it can also be either the precursor or the metabolite of glutamine. Unlike glutamine, which is the form of interorgan ammonia transport, glutamate metabolism is mostly compartmentalized within the cells, its interorgan exchanges being limited to a flux from liver to muscle. Summary: Glutamate catabolism is extremely intense in the splanchnic area, such that after a meal (rich in proteins) almost no glutamate appears in the systemic circulation. However, this process is saturable as after glutamate loading at a high dose level, glutamate appears dose-dependently in the circulation. This systemic glutamate appearance is blunted if glutamate is co-ingested with a carbohydrate source. Key Messages: The underlying reason for this highly specific metabolism is that glutamate plays a key role in nitrogen homeostasis, and the organism does all it can to limit the bioavailability of glutamate, which can be neurotoxic in excess. As glutamate is never eaten alone, its bioavailability will be limited if not negligible, and no adverse effects are to be expected in adult humans.

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Section: Pharmacokinetics Of Dietary Glutamatesupporting

confidence: 54%

“…There was no change in glutamate levels in red blood cells [19]. Some years later, Graham et al [24] conducted a similar study and obtained closely similar results.…”

Section: Pharmacokinetics Of Dietary Glutamatementioning

confidence: 66%

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Metabolism of Dietary Glutamate in Adults

Cynober

2018

Ann Nutr Metab

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“…However, since the carbohydrate content of the food administered with glutamate varied between groups (formula for infants and porridge for adults), the plasma glutamate levels are not directly comparable. Further, the plasma glutamate levels observed by Tung and Tung (20) in infants and adults were significantly lower than values we observed in normal adults administered 150 mg/kg body weight of MSG in water, where peak plasma glutamate levels reached 59.4 k 46.5 pmol/dl (16). Thus, the data of Tung and Tung (20) may be explained by the effect of carbohydrate on glutamate metabolism.…”

Section: Discussioncontrasting

confidence: 60%

Plasma Glutamate Concentrations in 1-Year-Old Infants and Adults Ingesting Monosodium L-Glutamate in Consommé

et al. 1986

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ABSTRACT. This study tested the hypothesis that infants metabolize glutamate more slowly than adults. Eight l-yrold infants ingested 160 ml of a beef consommi: providing monosodium L-glutamate at 0, 25, and 50 mg/kg body weight. Plasma glutamate and aspartate concentrations were measured sequentially for the next 2 h. The results were compared to values noted in nine adult subjects ingesting equivalent doses of monosodium L-glutamate in consomme. In adults, mean (+ SD) peak plasma glutamate concentrations were 5.59 f 1.56, 10.2 + 2.08, and 17.0 f The ability of human infants to metabolize MSG has been one area of concern in considering glutamate's safety as a food additive. Olney (1-3) postulated that human infants metabolized dicarboxylic amino acids more slowly than adults, and projected theoretical plasma glutamate concentrations for infants at much higher values than those for adults following glutamate ingestion.The present study directly tested this hypothesis by measuring the plasma glutamate and aspartate response in 1-yr-old infants fed a beef consommi containing graded doses of MSG. The results of these studies were compared with previously reported (4) plasma glutamate and aspartate values in normal adults administered equivalent doses of MSG in the same consomm6. MATERIALS AND METHODSEight infants (four male, four female) were studied. The proposed study was explained to at least one of the parents and informed, written consent was obtained. The protocol of the study was reviewed and approved by the Committee on Research Involving Human Subjects of the University of Iowa.Each child ingested 160 ml of beef consommC providing 0,25, and 50 mg/kg body weight of added MSG in a balanced crossover design. Each infant was randomly assigned to receive consommi providing either 0 or 25 mg MSG/kg body weight, followed by the other dose at least 1 wk later. After these two tests had been completed and the results evaluated, each infant ingested consommi providing MSG at 50 mg/kg body weight. All tests were begun at 0800 h following an overnight fast.The monohydrate of monosodium L-glutamate was purchased from a local grocery store (Accent International, Pet Incorporated, St. Louis MO). The soup was prepared from a special beef consommk base supplied by the Ajinomoto Company (Tokyo, Japan). The composition of the soup base is shown in Table 1. As noted in Table 1, 160 ml of reconstituted soup contained 37 mg of free glutamate, for a mean dose of 4.1 mg/kg body weight. Thus, the true final doses of MSG studied in these infants were 4.1, 29.1 and 54.1 mg/kg body weight.Each infant was assigned by random allocation into one of two equal groups that differed with respect to time of blood sampling. Since only four blood samples were obtained from each infant after dosing, two different sampling schedules were utilized so as to obtain samples during the entire absorptive period. Blood samples at each dose level were obtained from four infants at 0, 30, 60, and 120 min After ingestion of the consommG Blood samples from ...

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“…In the present study, amino acid concentrations were measured in blood plasma but not in erythrocytes. However, it was previously shown that erythrocyte glutamate and aspartate concentrations were not affected in humans after administration of large doses of MSG [31]. Although dicarboxylic amino acids are highly concentrated in red blood cells, it is generally considered that the exchanges with plasma proceed very slowly, and thus this intracellular pool contributes poorly to interorgan fluxes.…”

Section: Discussionmentioning

confidence: 99%

Portal Hyperglutamatemia after Dietary Supplementation with Monosodium Glutamate in Pigs

Blachier

Vaugelade

et al. 1999

Digestion

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The aim of the present work was to examine in pigs the effect of a dietary supplementation with the flavor enhancer monosodium glutamate (MSG) on intestinal amino acid metabolism. For this purpose, pigs weighing 60 ± 2 kg received a standard meal twice a day for 1 week, supplemented with either 10 g MSG per meal or, as control experiments, an isonitrogenous amount of glycine together with an equal amount of sodium in the form of NaCl, the animals being their own control in all experiments. At the end of this period, pigs received a MSG or glycine-NaCl-supplemented meal and samples of portal and arterial blood were collected for amino acid analysis in plasma. The results demonstrate after MSG supplementation rapid significant increases in glutamate concentration in the portal and arterial blood plasma after a test meal which resulted in a positive portoarterial difference. In comparison, after glycine-NaCl supplementation, glutamate concentrations were almost identical in portal and arterial plasma. Furthermore, significant increased aspartate concentration in the portal blood plasma was observed after MSG supplementation when compared with control experiments. When enterocytes were isolated at the end of the supplementation period from the jejunum and examined for their metabolic capacities towards L-glutamate and L-glutamine, it was found that metabolism did not differ according to the supplement used, with glutamate and glutamine being oxidized and transaminated at a similar level. It is concluded that the portal hyperglutamatemia observed shortly after the ingestion of a MSG- supplemented meal is likely due to the saturation of the intestinal capacity to metabolize glutamate with no measurable adaptation of the metabolic pathways controlling glutamate metabolism in enterocytes.

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Effect of carbohydrate on plasma and erythrocyte glutamate levels in humans ingesting large doses of monosodium L-glutamate in water

Cited by 41 publications

References 29 publications

Metabolism of Dietary Glutamate in Adults

Metabolism of Dietary Glutamate in Adults

Plasma Glutamate Concentrations in 1-Year-Old Infants and Adults Ingesting Monosodium L-Glutamate in Consommé

Portal Hyperglutamatemia after Dietary Supplementation with Monosodium Glutamate in Pigs

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