Disease relevance of glutamate

• Letter: Shuddering attacks in children: essential tremor and monosodium glutamate [1].
• Infusions of monosodium-L-glutamate into the rostral hypothalamus, believed to contain neurons mediating satiety, produced persistent hyperphagia and obesity, thus suggesting that a brain lesion had been produced [2].
• The MSG-treated mice showed increased body weight and decreased pituitary, thyroid, ovary, or testis weights [3].
• Unilateral injections into the RVL of the excitatory amino acid monosodium L-glutamate (50 pmol to 10 nmol), but not saline, caused transient dose-dependent and topographically specific elevations (maximum +71.6 +/- 4.9 mm Hg) of arterial blood pressure and tachycardia [4].
• Monosodium glutamate treatment, which induces weight gain and alters body growth in wild-type mice, further aggravates the growth defect of PPARgamma +/- mice [5].

Psychiatry related information on glutamate

• In contrast, peripheral administration of GLP-1 did not inhibit ANG II-induced drinking behavior in MSG-treated rats [6].
• The elevated plasma glucose and insulin in fed MSG treated mice fell rapidly with food deprivation [7].
• Prenatal monosodium glutamate (MSG) given through the mother's diet was found previously to cause behavioral changes in the offspring, including learning disabilities [8].
• To evaluate as accurately as possible the number of GCs able to phase shift the locomotor activity rhythm (LAR), neonatal hamsters treated with monosodium glutamate (MSG) were also used, an in vivo model which displays retinal degeneration and LAR normally entrained by light [9].
• We propose that the obesity-related changes in the feeding behavior of the MSG-treated obese mice were the result of missing leptin and insulin receptors in ARC and consequent altered neuropeptide signaling [10].

High impact information on glutamate

• Pulsatile, but not continuous GHRF also stimulates growth in animals made GHRF-deficient by neonatal monosodium glutamate treatment [11].
• These results show that the arcuate nucleus is the origin of the GRF-containing fibres that project to the median eminence and establish the MSG-treated rat as an in vivo model for studying growth hormone secretion in the absence of neurohumoral GRF [12].
• Specific depletion of immunoreactive growth hormone-releasing factor by monosodium glutamate in rat median eminence [12].
• MSG treatment results in the complete loss of GRF-immunoreactive cell bodies within this nucleus and provokes a selective disappearance of GRF-immunoreactive fibres in the median eminence [12].
• Decreased (58 to 80 percent) complement factor D activity, relative to lean controls, was observed as a common feature of several experimental models of obesity, including the ob/ob, db/db, and monosodium glutamate (MSG)-injected mouse and the fa/fa rat [13].

Chemical compound and disease context of glutamate

• However, mean peak plasma glutamate levels increased proportional to dose when MSG was added (10.2 +/- 2.00 and 17.0 +/- 8.06 mumol/dl at 25 and 50 mg/kg body weight respectively) [14].
• One meal had no additions while the other contained added monosodium L-glutamate and aspartame (each present at 34 mg/kg body weight) [15].
• The response of NPY-null mice to diet-induced obesity, chemically induced obesity (monosodium glutamate and gold thioglucose), and genetic-based obesity (lethal yellow agouti, Ay; uncoupling protein-diphtheria toxin transgenics, UCP-DT) were all normal [16].
• The monosodium glutamate fortification was the only intervention that resulted both in a significant reduction in clinical signs of xerophthalmia and in a significant rise in serum vitamin A levels [17].
• Correction of MSG-induced hypogonadism by physiological doses of estradiol corrected the abnormal bone resorptive activity in MSG-treated mice and uncovered their high bone mass phenotype [18].

Biological context of glutamate

• Females treated with MSG had fewer pregnancies and smaller litters, while males treated with MSG showed reduced fertility [3].
• Subchronic multiple dosing of NN2211 (200 microg/kg) twice daily for 10 days to normal and MSG-treated rats caused profound inhibition of food intake [19].
• A single bolus injection of NN2211 caused profound dose-dependent inhibition of overnight food and water intake and increased diuresis in both normal and MSG-treated rats [19].
• However, only those mice with 938 bp of the adipsin upstream regulatory region showed suppression of expression in adipose tissue in mice that were induced to become obese with monosodium glutamate [20].
• In order to investigate the asthma-provoking potential of the widely used flavor enhancer, monosodium L-glutamate (MSG), we challenged 32 subjects with asthma, a number of whom gave histories of severe asthma after Chinese restaurant meals or similarly spiced meals [21].

Anatomical context of glutamate

• Intraperitoneal injection of monosodium glutamate in neonatal rates resulted in a 90 percent loss of alpha-melanocyte-stimulating hormone in hypothalamic and extrahypothalamic areas of the brain, whereas the amount of hormone in the pituitary gland did not change [22].
• The taste of monosodium glutamate: membrane receptors in taste buds [23].
• Preferential interaction measurements between proteins and monosodium glutamate were carried out to arrive at an understanding of the mechanism of its strong effect on tubulin stability and self-assembly into microtubules [24].
• Effect of aspartame plus monosodium L-glutamate ingestion on plasma and erythrocyte amino acid levels in normal adult subjects fed a high protein meal [15].
• Effects of MSG on the neuroendocrine system [25].

Associations of glutamate with other chemical compounds

• In a controlled trial, fortification of commercially marketed monosodium glutamate (MSG) with vitamin A improved serum vitamin A levels of young children and the vitamin A content of breast milk of lactating women [26].
• Because abnormally high concentrations of glutamate can lead to overexcitation of neurones leading to cell damage and/or death, we investigated whether administration of growth hormone releasing peptide-6 attenuates monosodium glutamate-induced apoptosis in the rat hypothalamus and cerebellum [27].
• However, T and FT4 plasma levels were normal, and no apparent alterations were observed in testis structure of MSG rats [28].
• In vivo cerulenin treatment enhanced muscle CPT-1 activity in monosodium glutamate-treated arcuate nucleus lesioned mice but not in gold thioglucose-treated ventromedial hypothalamus lesioned mice [29].
• Substitutions of negatively charged (Glu195, Glu202, and Asp215) and polar residues (Asn214) of the CRD with alanine but not substitution of the Arg197 with glycine reduced the binding of SP-A to mannose-Sepharose beads and to MSG [30].

Gene context of glutamate

• The neuropeptide Y/agouti gene-related protein (AGRP) brain circuitry in normal, anorectic, and monosodium glutamate-treated mice [31].
• MSG treatment produced virtual elimination of NPY mRNA in the arcuate nucleus and a reduction of hypothalamic POMC mRNA, and led to elevated leptin [32].
• Significant increases in NMDA-R1, 2A and 2B subunits gene expression was also observed in ST and HP but not in CC, where only NMDA-R 2B was increased in MSG-treated rats [33].
• Although controversial, the evidence is consistent with an NMDA receptor serving as a primary taste transducer for monosodium glutamate (MSG), and a metabotropic glutamate receptor modulating the flavor-enhancing effect of MSG [34].
• This peak in pituitary Retn mRNA was unaffected by early weaning but was abolished by neonatal treatment with monosodium glutamate, suggesting that the basal hypothalamus regulates pituitary Retn [35].

Analytical, diagnostic and therapeutic context of glutamate

• In the ob/ob, UCP-DTA and MSG models, overexpression of ob mRNA is reversed by caloric restriction [36].
• Using a novel long-acting injectable GLP-1 derivative, NN2211, the acute and subchronic anorectic potentials of GLP-1 and derivatives were studied in both normal rats and rats made obese by neonatal monosodium glutamate treatment (MSG) [19].
• In the present study, the effects of intermittent GH treatment on liver CYP expression were studied in adult rats rendered GH deficient by neonatal administration of monosodium glutamate (MSG), which depletes circulating adult GH without the global loss of other pituitary-dependent hormones that is associated with hypophysectomy [37].
• OBJECTIVE: We conducted a multicenter, multiphase, double-blind, placebo-controlled study with a crossover design to evaluate reactions reportedly caused by MSG [38].
• We also observed that the preference for the monosodium glutamate solution was not induced in animals fed a low-protein diet [39].

References