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

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.     

Effect of naloxone on pancreatic and gastric endocrine function in response to carbohydrate and fat-rich test meals

The present study was designed to determine the effect of naloxone, a specific opiate receptor antagonist, on postprandial levels of insulin, glucagon, pancreatic polypeptide (PP), somatostatin-like immunoreactivity (SLI) and gastrin in response to carbohydrate and fat-rich test meals in a group of 6 healthy volunteers. The addition of naloxone to a meal consisting of 50 g sucrose dissolved in 200 ml water augmented the rise of plasma insulin levels significantly during the first 30 min after its ingestion and reduced the decrease of plasma glucagon. During the ingestion of a fat-rich meal in form of 200 ml cream naloxone reduced the rise in plasma insulin and pancreatic polypeptide and elevated glucagon levels during the last 30 min of the experimental period. When sucrose was dissolved in 200 ml cream the addition of naloxone augmented the postprandial rise of insulin levels between 15 and 60 min after ingestion of the meal and elicited an increase of plasma SLI and PP levels throughout the entire experimental period which indicates that post-prandial levels of insulin, glucagon, PP and SLI are modulated via endogenous opiate receptors during the ingestion of carbohydrate and fat test meals and that this effect depends on the composition of the ingested nutrients. These data raise the possibility that endogenous opiates participate in the regulation of postprandial insulin, glucagon, somatostatin and pancreatic polypeptide release not only in certain disease states as demonstrated recently for insulin secretion in type II diabetes mellitus but endogenous opiates may also be of importance under physiological conditions.     

Glutamate ingestion: the plasma and muscle free amino acid pools of resting humans

Monosodium glutamate (MSG) ingestion is known to increase plasma glutamate concentration, and MSG infusion stimulates insulin secretion. We investigated the impact of MSG ingestion on both the plasma and intramuscular amino acid pools. Nine postprandial adults ingested MSG (150 mg/kg) and rested for 105 min. Venous blood was sampled preingestion and then every 15 min; vastus lateralis muscle biopsies were taken preingestion and at 45, 75, and 105 min postingestion. Venous plasma glutamate and aspartate concentrations increased (P 相似文献   

Glutamate ingestion and its effects at rest and during exercise in humans.

Glutamate is central to several transamination reactions that affect the production of ammonia, alanine, glutamine, as well as TCA cycle intermediates during exercise. To further study glutamate metabolism, we administered 150 mg/kg body wt of monosodium glutamate (MSG) and placebo to seven male subjects who then either rested or exercised (15-min cycling at approximately 85% maximal oxygen consumption). MSG ingestion resulted in elevated plasma glutamate, aspartate, and taurine, both at rest and during exercise (P < 0.05), whereas most other amino acids were unchanged. Neither plasma alanine nor ammonia was altered at rest. During exercise and after glutamate ingestion, alanine was increased (P < 0.05) and ammonia was attenuated (P < 0.05). Glutamine was also elevated after glutamate ingestion during rest and exercise trials. MSG administration also resulted in elevated insulin levels (P < 0.05), which were parallel to the trend in C-peptide levels. Thus MSG can successfully elevate plasma glutamate, both at rest and during exercise. The plasma amino acid responses suggest that increased glutamate availability during exercise alters its distribution in transamination reactions within active muscle, which results in elevated alanine and decreased ammonia levels.     

Using the lymph fistula rat model to study the potentiation of GIP secretion by the ingestion of fat and glucose

Glucose-dependent insulinotropic polypeptide (GIP) is an important incretin produced in the K cells of the intestine and secreted into the circulating blood following ingestion of carbohydrate- and fat-containing meals. GIP contributes to the regulation of postprandial insulin secretion and is essential for normal glucose tolerance. We have established a method of assaying GIP in response to nutrients using the intestinal lymph fistula model. Administration of Ensure, a mixed-nutrient liquid meal, stimulated a significant increase in intestinal lymphatic GIP levels that were approximately threefold those of portal plasma. Following the meal, lymph GIP peaked at 60 min (P < 0.001) and remained elevated for 4 h. Intraduodenal infusions of isocaloric and isovolumetric lipid emulsions or glucose polymer induced lymph GIP concentrations that were four and seven times the basal levels, respectively. The combination of glucose plus lipid caused an even greater increase of lymph GIP than either nutrient alone. In summary, these findings demonstrated that intestinal lymph contains high concentrations of GIP that respond to both enteral carbohydrate and fat absorption. The change in lymphatic GIP concentration is greater than the change observed in the portal blood. These studies allow the detection of GIP levels at which they exert their local physiological actions. The combination of glucose and lipid has a potentiating effect in the stimulation of GIP secretion. We conclude from these studies that the lymph fistula rat is a novel approach to study in vivo GIP secretion in response to nutrient feeding in conscious rats.     

Resistance training restores metabolic alterations induced by monosodium glutamate in a sex-dependent manner in male and female rats

Despite resistance exercises being associated with health outcomes, numerous issues are still unresolved and further research is required before the exercise can faithfully be prescribed as medicine. The goal of this study was to investigate whether there are sex differences in resistance training effects on metabolic alterations induced by monosodium glutamate (MSG), a model of obesity, in male and female rats. Male and female Wistar rats received MSG (4 g/kg body weight/day, s.c.) from postnatal day 1 to 10. After 10 days from MSG administration, the rats were separated into two groups: MSG-sedentary and MSG-exercised. At postnatal day 60, the animals started a resistance training protocol in an 80 degrees inclined vertical ladder apparatus and performed it for 7 weeks. Control rats received saline solution and were divided in saline-sedentary and saline-exercised. Resistance training restored all plasma biochemical parameters (glucose, cholesterol, triglycerides, aspartate aminotransferase, and alanine aminotransferase) increased in male and female rats treated with MSG. The MSG administration induced hyperglycemia associated with a decrease in the skeletal muscle glucose transporter 4 (GLUT4) levels and accompanied by deregulation in proteins, G-6Pase, and tyrosine aminotransferase, involved in hepatic glucose metabolism of male and female rats. MSG induced dyslipidemia and lipotoxicity in the liver and skeletal muscle of male rats. Regarding female rats, lipotoxicity was found only in the skeletal muscle. The resistance training had beneficial effects against metabolic alterations induced by MSG in male and female rats, through regulation of proteins (GLUT2, protein kinase B, and GLUT4) involved in glucose and lipid pathways in the liver and skeletal muscle.     

Effect of nitric oxide inhibition on blood pressure and corticosterone responses in adult rats neonatally treated with glutamate

The role of nitric oxide (NO) in the regulation of blood pressure and hypothalamic-pituitary-adrenal function of adult rats treated with monosodium glutamate (MSG) during the neonatal period was investigated. Blood pressure and the heart rate were registered by a computerized system of direct blood pressure measurement through an indwelling cannula in the femoral artery. The inhibition of the activity of NO synthase by acute injection of Nomega-nitro-L-argininemethylester (L-NAME, 30 mg/kg, i.v.) to control rats produced a rise of blood pressure and a fall of heart rate. Both responses were reduced in MSG-treated rats. Repeated administration of L-NAME (50 mg/kg, i.p, two times daily for 4 days) increased BP in both groups of animals. Corticosterone concentrations in the plasma were significantly increased in response to repeated L-NAME administration in MSG-treated rats, while ACTH levels were similar in both groups of animals. These data suggest that some of the cardiovascular and endocrine changes in rats treated with MSG may be due to the abnormal function of the NO system.     

Changes in blood osmolarity,electrolytes, and metabolites among adult rats treated with a neurotoxic dose of MSG1

Adult rats were given large doses of MSG (4 g/kg) or isosmolar amounts of sodium chloride or L-alanine intraperitoneally or by forced intubation. Blood or plasma samples from these rats where assayed for osmolarity, hematocrit, pH, and concentrations of protein, sodium, potassium, chloride, calcium, magnesium, and urea nitrogen. Intraperitoneal MSG produced characteristic hypothalamic lesions; MSG by gavage failed to do so. Intraperitoneal MSG also caused major increases in plasma osmolarity, hemoconcentration, hypovolemia, alkalosis, hypernatremia, and uremia; plasma levels of chloride and potassium fell significantly. Administration of MSG by gavage caused much smaller changes in plasma osmolarity and sodium, and no significant changes in hematocrit, plasma protein or plasma urea nitrogen. Administration of sodium chloride or L-alanine (agents not known to produce the characteristics MSG brain lesions) caused some, but not all, of the metabolic changes seen after MSG. These observations suppot the hypothesis that the ability of large, concentrated doses of MSG to produce brain lesions in susceptible species involves a two-step process, i.e., initial damage to the blood-brain barrier for glutamate, followed by entry of the circulating amino acid into the extracellular space of the brain.     

Threonine Entry into Rat Brain After Diet-Induced Changes in Plasma Amino Acids

Abstract: Passage of amino acids across the blood-brain barrier is modified by the amino acid composition of the blood. Because blood amino acid concentrations respond to changes in protein intake, we have examined associations among diet, plasma amino acid patterns, and the rate of entry of threonine into the brain. Rats were adapted for 8 h/ day for 7–10 days to diets containing 6, 18 , or 50% casein before receiving a single, independently varied, final meal of a diet containing 0, 6, 18 , or 50% casein. After 4–7 h, they were anesthetized and infused intravenously with [¹⁴C]threonine for 5 min before plasma and brain samples were taken for determination of radioactivity and amino acid content. Plasma and brain threonine concentrations decreased as protein content increased in the diets to which the rats had been adapted. Plasma threonine concentrations increased twofold, from 1.6 to 3.0 m M , when rats adapted to 6% casein meals received a single 50% casein meal rather than a nonprotein meal; a fivefold increase, from 0.13 to 0.69 m M , occurred when rats had been previously adapted to 50% casein meals. Increasing the protein content of the final meal did not increase brain threonine concentrations. Highest and lowest rates of threonine entry into the brain occurred, respectively, in rats adapted to 6 and 50% casein meals. Changes in plasma threonine concentrations and threonine flux into brain reflected protein content of both pretreatment and final meals.     

Late effects of postnatal administration of monosodium glutamate on insulin action in adult rats

Early postnatal administration of monosodium glutamate (MSG) to rats induces obesity, hyperinsulinemia and hyperglycemia in adulthood, thus suggesting the presence of insulin resistance. We therefore investigated the effects of insulin on glucose transport and lipogenesis in adipocytes as well as insulin binding to specific receptors in the liver, skeletal muscle and fat tissues. An increase of plasma insulin, glucose and leptin levels was found in 3-month-old rats treated with MSG during the postnatal period. The attenuation of insulin stimulatory effect on glucose transport was observed in MSG-treated rats. Despite the lower basal and insulin-stimulated glucose uptake, the incorporation of glucose into lipids was significantly higher in MSG-treated rats, suggesting a shift in glucose metabolism towards lipid synthesis in fat tissue. Insulin binding to plasma membranes from the liver, skeletal muscle and adipocytes was decreased in MSG-treated rats. This is in agreement with the lower insulin effect on glucose transport in these animals. Furthermore, a decreased amount of GLUT4 protein was found in adipocytes from MSG-treated obese rats. The results demonstrated an attenuation of insulin effect on glucose transport due to a lower insulin binding and lower content of GLUT4 protein in MSG-treated rats. However, the effect of insulin on lipogenesis was not changed. Our results indicated that early postnatal administration of MSG exerts an important effect on glucose metabolism and insulin action in adipocytes of adult animals.     

Effects of monosodium glutamate on food acceptance and toxicity of selenium in rats

Food acceptance and toxic effects of feeding sodium selenite (Se) alone and in combination with monosodium glutamate (MSG), a taste enhancer were studied in the laboratory rat. Dose-dependent stimulation of daily food intake was observed with MSG offered in no-choice or bi-choice with the plain food. Consumption of pellets containing 0.05, 0.5 and 1.0% Se was significantly low than the plain or MSG containing pellets but their active ingredient was sufficient to cause mortality of rats. Food pellets containing both MSG and Se in no-choice feeding trial were not preferred by the rats, as their consumption remained low as compared to pellets containing only MSG. However, prior feeding on MSG containing pellets for two days increased the amount of intake of Se-containing pellets. No mortality of rats feeding on pellets containing different concentrations of MSG was recorded. Feeding on Se-containing pellets caused dose-dependent mortality on the third day of the trial. As compared to rats feeding on Se-containing pellets, the mortality rate was reduced in those provided Se in combination with MSG but the intake of active ingredient of Se in both these trials did not differ significantly. Decrease in death rate of rats feeding on Se in combination with MSG containing pellets suggested that addition of MSG to seleniferous food probably provide protection to some extent from the toxic effects of selenium. However, combination of excess doses of MSG and Se in food pellets caused mortality of all experimental animals.     

Effect of monosodium glutamate on apple leaf consumption by codling moth larvae

We have demonstrated that larvae of codling moth, Cydia pomonella (L) can successfully complete their first instar when fed apple leaves instead of fruit. Larvae fed leaves after hatching maximized their feeding intensity (about 320 g/larva/day) on day 2. Weight gain revealed a stereotypic sigmoid pattern that peaked on day 3. Although the maximum body weight of larvae fed leaves was 70–85% less than for larvae maintained on apples or on artificial diet, 100% of larvae fed leaves molted to the second instar 3–5 days after hatching. Our investigation revealed a diurnal pattern of leaf ingestion, and neonates' feeding intensity decreased significantly during the scotophase. We also demonstrated that monosodium glutamate (MSG) increased feeding on leaves by codling moth larvae. Depending on the duration of the bioassay, and larval age at time of initial exposure, 0.05 mg/ml and 0.1 mg/ml MSG increased apple leaf consumption by 25–60% over leaves alone. The effect of monosodium glutamate was best demonstrated during the first day following hatching. Exposure to MSG also accelerated molting to the second instar. Larvae exposed to MSG initiated consumption of leaf tissue significantly earlier than control neonates. The feeding stimulatory effect of MSG was not observed if exposure to this chemical was delayed until 3–4 h after hatch.The addition of feeding stimulants to pesticides that act via the alimentary tract may reduce the amount of active ingredients needed to maintain the efficacy of these formulations. Here, we postulate that first instar codling moth larvae are potential targets for treatment with pesticide formulations enhanced with monosodium glutamate.     

Monosodium glutamate exposure in the neonate alters hypothalamic and pituitary neuropeptide levels in the adult

Administration of monosodium glutamate (MSG) during the neonatal period in rats produced differential effects on the contents of various neuropeptides in the hypothalamus: beta-endorphin (beta-E) level was reduced by 70% while substance P (SP), neurotensin (NT) and Met5-enkephalin (ME) levels were not significantly changed (ME content of male rats was slightly reduced). The contents of ME, SP and NT in striatum and hippocampus were also unaffected by the same treatment. Male rats contain higher pituitary content of beta-endorphin-like immunoreactivity (beta-ELI) than female rats. MSG treatment reduced the pituitary content of beta-ELI and abolished the sex difference in beta-ELI level seen in the control rats. MSG treatment in the neonates by eliminating beta-E neurons while sparing ME neurons in the brain may be a useful tool for studying the different functions of these two separate opioid peptides.     

GIP and insulin release in relation to gastric emptying of a mixed meal in man

To clarify the role of GIP (gastric inhibitory polypeptide) as an incretin, we related temporally the gastric emptying of fat, protein and glucose to plasma levels of glucose, GIP and insulin in man. Five healthy volunteers with a multiple lumen duodenal tube ingested a mixed meal with phase-specific markers for the aqueous phase, liquid fat and the solid protein phase. Duodenal passage was determined by intraduodenal infusion of a second set of phase-specific non-absorbable markers. Plasma insulin rose rapidly from a basal value of 59 pM to 300 pM at 60 min, and then declined to reach basal levels after 180 min. By contrast, plasma GIP rose more slowly than insulin, from a basal value of 9.4 pM, and remained elevated, in the range of 14-18 pM, throughout the 240 min observation period. The time course of plasma insulin concentration paralleled gastric emptying of the aqueous phase, containing most of the meal's glucose (r = 0.952, P less than 0.001). The time course of plasma GIP concentrations paralleled the gastric emptying of fat and protein (r = 0.763-0.834; P less than 0.01-0.05). Plasma insulin concentrations showed no correlation to the rate of emptying of fat and protein (r = 0.142-0.420; n.s.) and to plasma levels of GIP (r = 0.365; n.s.). The threshold for plasma glucose at which GIP would exert an incretin effect only reached at one time point, 30 min after ingestion of the meal. Our findings of simultaneously tracked gastric emptying of meal nutrients, hormone release and plasma glucose levels do not support an important physiological role for GIP as an insulinotropic hormone after ingestion of mixed meals in man.     

Exogenous amino acids stimulate human muscle anabolism without interfering with the response to mixed meal ingestion

We sought to determine whether ingestion of a between-meal supplement containing 30 g of carbohydrate and 15 g of essential amino acids (CAA) altered the metabolic response to a nutritionally mixed meal in healthy, recreationally active male volunteers. A control group (CON; n = 6, 38 +/- 8 yr, 86 +/- 10 kg, 179 +/- 3 cm) received a liquid mixed meal [protein, 23.4 +/- 1.0 g (essential amino acids, 14.7 +/- 0.7 g); carbohydrate, 126.6 +/- 4.0 g; fat, 30.3 +/- 2.8 g] every 5 h (0830, 1330, 1830). The experimental group (SUP; n = 7, 36 +/- 10 yr, 87 +/- 12 kg, 180 +/- 3 cm) consumed the same meals but, in addition, were given CAA supplements (1100, 1600, 2100). Net phenylalanine balance (NB) and fractional synthetic rate (FSR) were calculated during a 16-h primed constant infusion of L-[ring-2H5]phenylalanine. Ingestion of a combination of CAA supplements and meals resulted in a greater mixed muscle FSR than ingestion of the meals alone (SUP, 0.099 +/- 0.008; CON, 0.076 +/- 0.005%/h; P < 0.05). Both groups experienced an improvement in NB after the morning (SUP, -2.2 +/- 3.3; CON, -1.5 +/- 3.5 nmol x min(-1) x 100 ml leg volume(-1)) and evening meals (SUP, -9.7 +/- 4.3; CON, -6.7 +/- 4.1 nmol x min(-1) x 100 ml leg volume(-1)). NB after CAA ingestion was significantly greater than after the meals, with values of 40.2 +/- 8.5 nmol x min(-1) x 100 ml leg volume(-1). These data indicate that CAA supplementation produces a greater anabolic effect than ingestion of intact protein but does not interfere with the normal metabolic response to a meal.     

Ghrelin response to protein and carbohydrate meals in relation to food intake and glycerol levels in obese subjects

Obese subjects have lower basal and an attenuated decrease of postprandial plasma ghrelin following carbohydrate-rich meals, while the response to protein is unknown. Therefore, plasma ghrelin levels were examined after ingestion of satiating amounts of a protein- or carbohydrate-rich meal in relation to food and energy intake and hunger/satiety ratings in 30 obese subjects followed 240 min later by ad lib sandwiches. Food intake and hunger/satiety ratings were identical while energy intake was significantly greater after bread (861 +/- 62.7 vs. 441 +/- 50.4 kcal, p < 0.001). Second meal food and energy intake were not different. Ghrelin decreased after bread, but increased by 50 pg/ml (p < 0.001) after meat. The corresponding increase of insulin was 55 vs. 9 microU/ml (p < 0.001). Glycerol levels decreased significantly less after the protein meal compared to carbohydrates. After protein glycerol was significantly correlated to the rise of ghrelin but not insulin. These data demonstrate that, in obese subjects, protein has no different satiating effect than carbohydrate despite divergent ghrelin levels. Energy intake corresponds to energy density of the respective food items. Ghrelin response to both meals is qualitatively similar but quantitatively attenuated compared to normal weight subjects. The relationship between ghrelin and glycerol would support recent observations of a possible role of ghrelin in fat metabolism.     

Effect of monosodium glutamate on apoptosis and Bcl-2/Bax protein level in rat thymocyte culture

Monosodium glutamate (MSG), the sodium salt of glutamate, is commonly used as a flavor enhancer in modern nutrition. Recent studies have shown the existence of glutamate receptors on lymphocytes, thymocytes and thymic stromal cells. In this study, we evaluated the in vitro effect of different MSG concentrations on rat thymocyte apoptosis and expression of two apoptosis-related proteins, Bcl-2 and Bax. Rat thymocytes, obtained from male Wistar rats, were exposed to increasing concentrations of MSG (ranging from 1 mM to 100 mM) for 24 h. Apoptosis was detected using the Annexin V-FITC/PI apoptosis detection kit and cells were analyzed using a flow cytometer. Expression of Bcl-2 and Bax proteins were determined with flow cytometry using respective monoclonal antibodies. Exposure to MSG resulted in a dose-dependent decrease in cell survival (as determined by trypan blue exclusion method). Annexin V-FITC/PI also confirmed that MSG increased, in a dose-dependent manner, apoptotic cell death in rat thymocyte cultures. MSG treatment induced downregulation of Bcl-2 protein, while Bax protein levels were not significantly changed. Our data showed that MSG significantly modulates thymocyte apoptosis rate in cultures. The temporal profile of Bcl-2 and Bax expression after MSG treatment suggests that downregulation of Bcl-2 protein and the resulting change of Bcl-2/Bax protein ratio may be an important event in thymocyte apoptosis triggered by MSG.     

Effect of neonatal treatment with monosodium glutamate on vasopressin release during foot shock stress in the rat

Several lines of evidence indicate that beta-endorphin inhibits the release of vasopressin during foot shock-induced stress in the rat. This study was to evaluate the relative importance of the hypothalamic versus the pituitary pool of beta-endorphin. Neonatal treatment with monosodium glutamate (MSG) reduced drastically the content of beta-endorphin-like immunoreactivity (beta-EI) of hypothalamus but not the beta-EI concentration in the pituitary; the content of vasopressin in the hypothalamus and the pituitary was not altered by MSG treatment. MSG treatment had no effect on the plasma vasopressin response to inescapable electric foot shock stress, when compared to controls. Naloxone enhanced vasopressin release during stress both in MSG-treated rats and in controls. These results suggest that hypothalamic beta-endorphin is not involved in the control of vasopressin release during foot shock-induced stress in the rat.     

Effect of chronic ethanol or acetaldehyde on hepatic alcohol and aldehyde dehydrogenases, aminotransferases and glutamate dehydrogenase

Ethanol or acetaldehyde orally administered (15% and 2% respectively in drinking water) to male Wistar rats for three months induced alterations in the main liver enzymes responsible for ethanol metabolism, aspartate and alanine aminotransferases and NAD glutamate dehydrogenase. Ethanol produced a significant decrease in the activity of soluble alcohol dehydrogenase, while acetaldehyde induced alterations both in soluble and mitochondrial aldehyde dehydrogenases: soluble activity was significantly higher than in the control and ethanol-treated groups, and mitochondrial activity was significantly diminished. Both soluble aspartate and alanine aminotransferases showed pronounced increases by the chronic effect of acetaldehyde, while mitochondrial activities were practically unchanged by the effect of ethanol or acetaldehyde. Mitochondrial NAD glutamate dehydrogenase showed a rise in its activity both by the effect of chronic ethanol and acetaldehyde consumption. The level of metabolites assayed in liver extracts showed marked differences between ethanol and acetaldehyde treatment which indicates that ethanol produced a remarkable increase in glutamate, aspartate and free ammonia together with marked decrease in pyruvate and 2-oxoglutarate concentrations. Acetaldehyde consumption induced a significant decrease in 2-oxoglutarate and pyruvate concentrations. These observations suggest that ethanol has an important effect on the urea cycle enzymes, while the effect of acetaldehyde contributes to the impairment of the citric acid cycle.     

Influence of monosodium glutamate on circadian rhythms of lipid peroxidation products and antioxidants in rats

Monosodium glutamate (MSG) was administrated subcutaneously for 60 days to Wistar rats and 24h rhythms of thiobarbituric acid reactive substances (TBARS) and antioxidants such as reduced glutathione, superoxide dismutase and catalase were studied. MSG treatment was found to advance TBARS and to delay the acrophases of GSH and catalase. Amplitude and mesor values of these rhythms were found to be altered during MSG treatment. As glutamate levels in brain were found to be significantly increased (in MSG), we hypothesize that increased glutamate levels in brain could alter these biochemical rhythms probaly by modulating the transmission in several areas/nuclei in brain.