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Weaning: Why, When and What?
Published in Frank Falkner, Infant and Child Nutrition Worldwide:, 2021
Glutamic acid is present in most nutrients, either free or bound to peptides and proteins. The average intake of glutamic acid depends, of course, on the type of food. The concentration of glutamate in human milk is 10 times higher than in rodent milk and about five times that of cow’s milk.
Micronutrient Supplementation and Ergogenesis — Amino Acids
Published in Luke Bucci, Nutrients as Ergogenic Aids for Sports and Exercise, 2020
MSG has been shown to be more toxic than glutamic acid in subjects with “Chinese Restaurant Syndrome”.730 Nausea and vomiting have been known to occur when serum glutamic acid levels are increased 20-fold.730 Perhaps p.o. administration of glutamic acid, but not MSG, would alleviate nausea. These studies have not yet been performed in conjunction with physical performance.
Inherited Differences in Alpha1-Antitrypsin
Published in Stephen D. Litwin, Genetic Determinants of Pulmonary Disease, 2020
Jeppson [82] also removed sialic acid from his protein but then treated it with CNBr, Eight major fragments were isolated by isoelectric focusing and gel chromatography. One major peptide, fragment "C," which showed a clear difference in charge on isoelectric focusing was digested with thermolysin. The hydrolysate was fingerprinted and a peptide difference between M and Ζ alpha1-antitrypsin was found which was due to a substitution of lysine for glutamic acid in Ζ protein. They did not find a second change of glutamic acid to glutamine as did Yoshida et al. [81].
A Nutritional Blend Suppresses the Inflammatory Response from Bronchial Epithelial Cells Induced by SARS-CoV-2
Published in Journal of Dietary Supplements, 2023
José Roberto Mateus-Silva, Carlos Rocha Oliveira, Maysa Alves Rodrigues Brandao-Rangel, Anamei Silva-Reis, Fabiana Regina da Silva Olimpio, Lucas dos Santos Zamarioli, Flavio Aimbire, Rodolfo P. Vieira
Glutamic acid, an acidic amino acid that is another component of the nutritional blend, exerts anti-inflammatory and antioxidant effects on a model of intestinal inflammation (39). In fact, supplementation with glutamic acid inhibits the apoptosis of intestinal epithelial cells induced by increased levels of reactive oxygen species (39). Therefore, we hypothesize that in our in vitro study with BEAS-2B bronchial epithelial cells, some of the protective effects of the nutritional blend may be attributed to the effects of glutamic acid present in the formula. However, this hypothesis should be tested in another study. On the other hand, these possible effects of glutamic acid present in the formula of the nutritional blend are reinforced, as the nutritional blend inhibited the release of proinflammatory cytokines while increasing the release of the anti-inflammatory cytokine IL-10 from BEAS-2B cells.
Major component causing neurological toxicity in acute glufosinate ammonium poisoning: determination of glufosinate, 1-methoxy-2-propanol, and ammonia in serum and cerebrospinal fluid
Published in Clinical Toxicology, 2022
Seonghoon Yeon, Sung Hwa Kim, Juhyun Sim, Sunchun Kim, Yoonsuk Lee, Hyun Kim, Yong Sung Cha
The mechanism of this increase in serum ammonia concentration in GLA poisoning is not clearly understood. Glufosinate is available as an ammonium salt and thus may be a source of ingested free ammonia. However, there is no information regarding neurological effects of ammonia or ammonium compounds in humans after oral exposure [20]. Glufosinate is a glutamate analogue that reportedly inhibits GS in plants and blocks the synthesis of glutamine from glutamate and ammonia [9]. Glufosinate has also been reported to inhibit the activity of GS in vitro [21] through affecting the metabolic pathway of glutamic acid and the glutamic acid receptors in the brain [22]. Therefore, inhibition of GS by serum glufosinate in the acute phase of human GLA poisoning might lead to a further increase in ammonia levels in the brain, by inhibiting the already saturated GS. In animal studies, the metabolism of GLA was limited (up to 30% of the absorbed dose) and the main urinary and tissue residues were 3-[hydroxy(methyl)phosphinoyl] propionic acid, methylphosphinico butanoic acid, and 2-hydroxy-4-methylphosphinicobutanoic acid. In faeces, significant concentrations (up to 10%) of N-acetylglufosinate were detected, and there is no evidence of this metabolite having pathological findings suggesting a relationship with neurotoxicity [23]. A comparative study of the inhibition of GS in tissues from groups of ten male rats given diets containing N-acetylglufosinate and GLA was performed. The results indicated that orally administered GLA is approximately ten times more potent at inhibiting GS than N-acetylglufosinate [23].
Emerging drugs for the prevention of migraine
Published in Expert Opinion on Emerging Drugs, 2021
Oyindamola Ogunlaja, Nazia Karsan, Peter Goadsby
There is extensive evidence for the role of glutamate in migraine pathophysiology. Studies have shown increased plasma and CSF levels of glutamate ictally and interictally in migraine patients [84–87]. Increased salivary levels of glutamate have also been found in patients with episodic and chronic migraine [88,89]. Monosodium glutamate, the sodium salt of glutamic acid has been suggested to trigger headaches [90,91]. In terms of migraine and the group I metabotropic glutamate receptors – mGluR5 has undergone more investigation than mGluR1. mGluR5 is present in trigeminal sensory afferents [92], the trigeminal ganglion [93], and the TCC [94,95]. The receptor is known to be involved in central sensitization, hence creating hyperalgesia and allodynia [81,82,96]. A recent study [97] showed that mGluR5 may contribute to the central sensitization of chronic migraine through regulation of synaptic plasticity via protein kinase C/N-methyl-D-aspartate receptor subtype 2B (NR2B) signaling, making it a potential therapeutic target for chronic migraine.