Effect Of Monosodium L-glutamate Research Articles

Monosodium L-glutamate and fats change free fatty acid concentrations in intestinal contents and affect free fatty acid receptors express profile in growing pigs.

BackgroundObesity and its related metabolic syndrome continue to be major public health problems. Monosodium L-glutamate (MSG) may cause metabolic diseases such as obesity. Meanwhile, the Chinese population has undergone rapid transition to a high-fat diet. There is little information available on the effect of MSG and fat alone, or in combination, on free fatty acids (FFAs), lipid metabolism and FFA receptors.ObjectiveThe aim of this study was to evaluate the effects of MSG and fat alone, or in combination, on intestinal luminal FFAs and expression of gastrointestinal FFA receptors. The aim was also to test whether dietary fat and/or MSG could affect expression of genes related to fatty acid metabolism.DesignA total of 32 growing pigs were used and fed with four iso-nitrogenous and iso-caloric diets. Pigs in the four treatments received diets with one of two fat concentrations levels (4.4 and 9.4%) and one of two MSG dose levels (0 and 3%), in which most of the fat were brought by soybean oil. The concentration of short chain fatty acids (SCFAs) in cecum and colon, long chain fatty acids (LCFAs) in ileum, cecum and colon, and FFAs receptors expression in hypothalamus and gastrointestinal tract were determined.ResultsMSG and/or fat changed intestinal luminal SCFAs, levels of LCFAs, and showed an antagonistic effect on most of LCFAs. Simultaneously, MSG and/or fat decreased the expression of FFA receptors in hypothalamus and gastrointestinal tract. MSG and/or fat promoted fat deposition through different ways in back fat.ConclusionOur results support that MSG and/or fat can alter intestinal luminal FFAs composition and concentration, especially LCFAs, in addition, the expression of FFA receptors in ileum and hypothalamus could be decreased. Moreover, MSG and/or fat can promote protein deposition in back fat, and affect the distribution and metabolism of fatty acids in the body tissues and the body’s ability to perceive fatty acids; these results provide a reference for the occurrence of fat deposition and obesity caused by high-fat and monosodium glutamate diet.

The Effect of Monosodium L-Glutamate (MSG) Treatment for Short and Long Terms to The Semen Quality of Adult Male Rats

This study was conducted to investigate the effect of MSG treatment for short and long term on the semen quality of adult male rats. Twelve male adult Wistar rats with 200-300g of body weight (BW) and 3-4 month of age were used in this study. The animals were divided randomly into 3 groups. M0 was used as a control, M1 and M2 were given with MSG 4mg/gBW for 15 and 45 days respectively. The experimental animals were sacrificed on the days 16 th (to M1 group) and 46 th (to M0 and M2 groups). The epididymis was isolated and semen quality (motility, viability, concentration, and abnormality of sperm) was evaluated. The results showed motility and concentration of M1 and M2 were not significantly decreased compared to M0. MSG treatment also significantly reduced viability and increased abnormality of sperm. Analysis of sperm abnormality character shows that the use of long-term MSG caused a formation of the primary abnormality (round and double head sperm) and increased the secondary abnormality (bent neck, curve tail, coiled tail, headless, and tailless) compared to control. Conclusion, semen quality decreases with consumed MSG for the long term. For this reason, reconsidering the use of MSG as an enhancer for the teste of food is very important. Keywords: epididymis, Monosodium L-Glutamate, semen quality.

Dietary consumption of monosodium L‐glutamate induces adaptive response and reduction in the life span of Drosophila melanogaster

Adaptive response is the ability of an organism to better counterattack stress-induced damage in response to a number of different cytotoxic agents. Monosodium L-glutamate (MSG), the sodium salt of amino acid glutamate, is commonly used as a food additive. We investigated the effects of MSG on the life span and antioxidant response in Drosophila melanogaster (D.melanogaster). Both genders (1 to 3days old) of flies were fed with diet containing MSG (0.1, 0.5, and 2.5-g/kg diet) for 5days to assess selected antioxidant and oxidative stress markers, while flies for longevity were fed for lifetime. Thereafter, the longevity assay, hydrogen peroxide (H2 O2 ), and reactive oxygen and nitrogen species levels were determined. Also, catalase, glutathione S-transferase and acetylcholinesterase activities, and total thiol content were evaluated in the flies. We found that MSG reduced the life span of the flies by up to 23% after continuous exposure. Also, MSG increased reactive oxygen and nitrogen species and H2 O2 generations and total thiol content as well as the activities of catalase and glutathione S-transferase in D.melanogaster (P<.05). In conclusion, consumption of MSG for 5days by D.melanogaster induced adaptive response, but long-term exposure reduced life span of flies. This study may therefore have public health significance in humans, and thus, moderate consumption of MSG is advocated by the authors.

Numerical Evaluation of Efficacy of Glutamate on Gastrointestinal Motility: Rapid MRI Study.

The umami taste amino acid, glutamate acts as a signaling molecule in multiple cellular systems in the body, including the brain and gastrointestinal tract. Therefore, glutamate may affect appetite by modulating gastrointestinal motility as well as through taste perception. In this study, we examined the effect of glutamate on gastric emptying and duodenal motility, by using rapid magnetic resonance imaging (MRI). Ten healthy male volunteers participated in the measurements. Abdominal coronal MR images were successively acquired after ingestion of a liquid meal with and without monosodium L-glutamate (MSG). Image analysis was performed with a homemade segment software, in which respiratory motions were cancelled automatically by minimizing an energy function, thereby allowing participants breathe freely during MRI measurements. In two out of 10 participants, gastric emptying slowed down, while in the remaining eight participants, gastric residual volume decreased to 84% without MSG, and to 73% with MSG after 60 min. The inclusion of MSG enhanced duodenal motility, judging from changes in, 1) the magnitude of the duodenal area, 2) the center of gravity, and 3) the mean velocity of the wall motions. The third parameter most significantly indicated the excitatory effect of MSG on duodenum motility (3-7 fold increase). In conclusion, the present observations of rapid MRI indicate that MSG accelerates gastric emptying by facilitating duodenal motility, at least in healthy subjects with positive responses to MSG. This suggests the possible use of MSG as a prokinetic nutrient for improving the quality of life in hospitalized patients after a clinical assessment.

Monosodium L-glutamate and dietary fat exert opposite effects on the proximal and distal intestinal health in growing pigs.

The Chinese population has undergone rapid transition to a high-fat diet. Furthermore, monosodium L-glutamate (MSG) is widely used as a flavour enhancer in China. Previous studies have reported that high-fat diet modifies intestinal metabolism and physiology. However, little information is available on the effects of oral MSG on intestine, and no study focus on the interaction of dietary fat and MSG for intestinal health. The aim of the present study was to evaluate the effects of MSG and dietary fat on intestinal health in growing pigs, and to try to identify possible interactions between these 2 nutrients for such effects. A total of 32 growing pigs were used and fed with 4 isonitrogenous and isocaloric diets (basal diet, high-fat diet, basal diet with 3% MSG and high fat diet with 3% MSG). Parameters related to reactive oxygen species metabolism, epithelial morphology, pro-inflammation factors and tight junction protein expression and several species of intestinal microbe were measured. Overall, dietary fat and MSG had detrimental effects on several of the physiological and inflammatory parameters measured in the proximal intestine, while exerting beneficial effects on the distal intestine in growing pigs, with generally antagonistic effects. These results may be of particular relevance for nutritional concerns in patients with intestinal diseases.

Gastric emptying and duodenal motility upon intake of a liquid meal with monosodium glutamate in healthy subjects.

Glutamate is thought to serve as a special signal for gut functions. We investigated the effects of monosodium l‐glutamate (MSG) on gastric emptying and duodenal motility. Ten healthy male volunteers underwent rapid magnetic resonance imaging (MRI) of the abdomen. Coronal images were successively acquired after ingestion of liquid meal (200 kcal in 200 mL: 9 g protein, 28.4 g carbohydrate, 5.6 g fat, 370 mg Na+) with and without 0.5% MSG. During the acquisition of MRI, participants breathed freely. In all participants, the gastric residual volume gradually decreased to 80.1 ± 14.2% without MSG and to 75.9 ± 14.3% with MSG after 60 min (P = 0.45 between the groups, n = 10). In two of 10 participants, gastric emptying slowed down significantly, whereas in the remaining eight participants, gastric residual volume decreased to 84.0 ± 13.1% without MSG, and to 73.0 ± 14.6% with MSG after 60 min (P = 0.015, n = 8). There was no difference in the shape of the stomach between groups. In four of the eight participants responding positively to MSG, the duodenum wall was sufficiently identified to quantify the motions. The inclusion of MSG enhanced duodenal motility, judging from changes in (1) the magnitude of the duodenal area, (2) the center of gravity, and (3) the mean velocity of the wall motions. The third parameter most significantly indicated the excitatory effect of l‐glutamate on duodenum motility (~ three‐ to sevenfold increase during 60 min, P < 0.05, n = 4). These results suggest that MSG accelerates gastric emptying by facilitating duodenal motility, at least in subjects with positive responses to MSG.

Histological and immunohistochemical study of the effect of monosodium l-glutamate on the jejunal mucosa of adult albino rat and the possible role of propolis

Histological and immunohistochemical study of the effect of monosodium l-glutamate on the jejunal mucosa of adult albino rat and the possible role of propolis

The Acute and Chronic Effects of Monosodium l-Glutamate on Serum Iron and Total Iron-Binding Capacity in the Jugular Artery and Vein of Pigs

We analyzed the effects of acute and chronic oral administration of monosodium L-glutamate (MSG) on serum iron (Fe) levels and total iron-binding capacity (TIBC) in piglets. In the first experiment, 12 piglets were randomly assigned to two groups: one fed a standard diet (SD) and the other fed an SD containing MSG (10g/kg). On day 30, serum, liver, kidney, and spleen samples were collected to determine the Fe levels. In the second experiment, six pigs were surgically fitted with a catheter in the jugular artery and vein to investigate the dynamic changes of serum Fe and TIBC. Blood samples were taken from each pig via the catheter every 30min, for a period of 4h. The results show that MSG increases Fe levels in the spleen (P < 0.05) and in serum obtained from the jugular artery (P < 0.01). In addition, TIBC in serum obtained from the jugular artery demonstrated an increasing trend in pigs fed the MSG diet; however, this trend was not observed in the jugular vein. In conclusion, MSG increases Fe retention by enhancing TIBC in serum.

Contribution of Umami Substance to Swallowing

Reflecting progressive aging of society, many special diets for patients suffering from swallowing disorders (i.e. dysphagia diets) have been developed. Texture modification for less risk of aspiration is one of the important elements in dysphagia diets from the viewpoint of safety assurance. However, no attempt has been done to add chemicals to such diets to facilitate swallowing initiation. For this, sensory inputs from the oropharynx play an important role in swallow initiation. Animal studies showed that stimulation by umami taste is effective stimulus of this area. Therefore, to study the effect of umami taste on swallow initiation in humans, we examined the effect of application of Monosodium L-Glutamate (MSG) solution as an umami taste to the oropharynx on the latency of the swallow reflex evoked by electrical stimulation of the oropharynx. Distilled water (DW) and 0.15 M sodium chloride (NaCl) solution (saline) were used as vehicles of MSG. Each of the DW, saline, 0.1 M MSG dissolved with DW (MSGDW) and 0.1 M MSG dissolved with saline (MSG-saline) were slowly injected approximately 1 s prior to electrical stimulation. The amount of each solution was 0.1 ml. No swallow was evoked when each of the solutions was applied to the posterior wall of the oropharynx without electrical stimulation, and the subjects could not discriminate the solutions. Results showed that application of DW to the oropharynx shortened the latency of the swallow reflex, but saline application elongated the latency of the reflex. Also, application of MSG-saline solution counteracts the elongation of the latency induced by saline application. This counteractive effect of MSG was concentrationdependent. Above findings suggest that using MSG as a food additive with NaCl (i.e. salty taste) may serve not only as a flavor enhancer but also as an enhancer of swallow initiation.

Monosodium glutamate stimulates secretion of glucagon‐like peptide‐1 and reduces postprandial glucose after a lipid‐containing meal

Monosodium l-glutamate (MSG) is known to influence the endocrine system and gastrointestinal (GI) motility. The mechanism of postprandial glycemic control by food in the GI tract is mostly unknown and of great interest. To investigate the effect of MSG on glucose homeostasis, incretin secretion and gastric emptying in humans after a lipid-containing meal. Thirteen healthy male volunteers (mean age, 25.5 years) and with no Helicobcter pylori infection were enrolled. A 400 mL (520 kcal) liquid meal with MSG (2 g, 0.5% wt:vol) or NaCl (control) was ingested in a single-blind placebo-controlled cross-over study. Blood glucose, serum insulin, plasma glucagon, plasma glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide were measured. Gastric emptying was monitored by a 13C acetate breath test. Postprandial symptoms were assessed on a visual analogue scale. The 30-min postprandial glucose concentration was significantly reduced by adding MSG to the test meal. The area under the glucose concentration vs. time curve (0-60 min) was also significantly reduced by adding MSG (40.6 ± 3.51 mg·1 hr/dL with MSG vs. 49.2 ± 3.86 mg·1 hr/dL with NaCl, P = 0.047), whereas, the 30-min postprandial plasma GLP-1 level was significantly increased (58.1 ± 15.8 pmol/L with MSG vs. 13.4 ± 15.8 pmol/L with NaCl, P = 0.035). MSG did not affect the half gastric emptying time or postprandial symptoms. Monosodium l-glutamate improved early postprandial glycaemia after a lipid-containing liquid meal. This effect was not associated with a change in gastric emptying, but was possibly related to stimulation of glucagon-like peptide-1 secretion.

Intragastric monosodiuml-glutamate stimulates motility of upper gut via vagus nerve in conscious dogs

Monosodium l-glutamate (MSG) is a substance known to produce the umami taste. Recent studies indicate that MSG also stimulates a variety of activities in the gastrointestinal tract through its receptor in the gut, but no study has reported the activity in conscious large experimental animals. The aim of our study was to investigate whether direct intragastric MSG stimulates gut motility and to identify the mechanism in conscious dogs. Contractile response to intraluminal injection of MSG was studied in the fed and fasted states by means of chronically implanted force transducers. MSG (5, 15, 45, and 90 mM/kg) dissolved in water was injected into the stomach and duodenum in normal and vagotomized dogs. MSG solution was administered into the stomach before feeding, and gastric emptying was evaluated. Several inhibitors of gastrointestinal motility (atropine, hexamethonium, and granisetron) were injected intravenously before MSG administration to the stomach. The effect of MSG was investigated in Pavlov (vagally innervated corpus pouch), Heidenhain (vagally denervated corpus pouch), and antral pouch (vagally innervated) dogs. Upper gut motility was significantly increased by intragastric MSG but not significantly stimulated by intraduodenal MSG. Intragastric MSG (45 mM/kg) stimulated postprandial motility and accelerated gastric emptying. MSG-induced contractions were inhibited by truncal vagotomy, atropine, hexamethonium, and granisetron. Gut motility was increased by intrapouch injection of MSG in the Pavlov pouch, but it was not affected in the Heidenhain or antral pouch dogs. We conclude that intragastric MSG stimulates upper gut motility and accelerates gastric emptying. The sensory structure of MSG is present in the gastric corpus, and the signal is mediated by the vagus nerve.

MSG intake suppresses weight gain, fat deposition, and plasma leptin levels in male Sprague–Dawley rats

Monosodium l-glutamate (MSG), an umami taste substance, may be a key molecule coupled to a food intake signaling pathway, possibly mediated through a specific l-glutamate (GLU) sensing mechanism in the gastrointestinal tract. Here we investigated the effect of the spontaneous ingestion of a 1% MSG solution and water on food intake and body weight in male Sprague-Dawley rats fed diets of varying caloric density, fat and carbohydrate contents. Fat mass and lean mass in the abdomen, blood pressure, and several blood metabolic markers were also measured. Rats given free access to MSG and water showed a high preference (93-97%) for the MSG solution, regardless of the diet they consumed. Rats ingesting MSG had a significantly smaller weight gain, reduced abdominal fat mass, and lower plasma leptin levels, compared to rats ingesting water alone. Naso-anal length, lean mass, food and energy intakes, blood pressure, blood glucose, and plasma levels of insulin, triglyceride, total cholesterol, albumin, and GLU were not influenced by the ingestion of the MSG solution. These same effects were observed in a study of adult rats. Together, these results suggest that MSG ingestion reduces weight gain, body fat mass, and plasma leptin levels. Moreover, these changes are likely to be mediated by increased energy expenditure, not reduced energy intake or delayed development. Conceivably, these effects of MSG might be mediated via gut GLU receptors functionally linked to afferent branches of the vagus nerve in the gut, or the afferent sensory nerves in the oral cavity.

Release of hypothalamic norepinephrine during MSG intake in rats fed normal and nonprotein diet

Effects of monosodium l-glutamate (MSG) solution (0.06 M) on interstitial levels of norepinephrine (NE) were measured in the lateral hypothalamus (LH). Wistar male rats, housed in standard operant boxes, were fed either normal or nonprotein diet for 3 days. Beside a daily bar-mediated drinking session (75 min), animals were without access to fluids. Microdialysates, collected from the LH during the 75 min of drinking, were analyzed using high-pressure liquid chromatography. No significant responses of the LH NE to the drinking of distilled water, MSG, NaCl (0.06 M), and glucose solution (0.6 M) were found in normally fed rats. However, a specific decline in LH NE release was detected during MSG solution-drinking in rats fed nonprotein diet. As MSG preference indicates protein intake, it is possible that LH NE is, at least partially, one of the brain signals that relate MSG preference to dietary protein intake.

Lack of carcinogenicity of monosodium l-glutamate in Fischer 344 rats

Monosodium l-glutamate (MSG) was administered to groups of 50 male and 50 female Fischer 344 rats in the diet at levels of 0, 0.6, 1.25, 2.5 and 5.0% for a 2-yr period. Survival of dosed and control rats of both sexes was comparable, although animals receiving 5.0% MSG showed a trend towards (or significant) growth retardation. Urinary biochemistry values indicated increased pH and Na + levels and decreased K + in rats of both sexes given 2.5 or 5.0%. However, no significant increases in proliferative or neoplastic lesion development in the urinary tract were observed in any MSG-treated animals. In addition, occurrences of neoplastic lesions in other organs did not differ between treated and control groups. The present study thus did not demonstrate any long-term carcinogenic effect of MSG administered to rats at levels up to 5.0% in the diet.

Effects of monosodium l glutamate on diet palatability and piglet performance during the suckling and weaning periods

ABSTRACTThe effect of monosodium L glutamate (MSG) on diet palatability and piglet performance during the suckling and weaning periods was studied in the course of five successive experiments involving a total of 230 litters during the suckling period and 120 pens of seven piglets during the post-weaning period. During the suckling period, the addition of 5 g MSG per kg diet led to a significant 0·36 proportional increase of creep food intake from the 18th day post farrowing. However, no increase in weaning weight was observed subsequent to the intake of the diet with added MSG. Moreover, in an experiment where MSG was added with an associated commercial flavour, no flavour enhancing effect of MSG was detectable. Few health problems were encountered at weaning and the number of scouring piglets was not related to one particular diet. During the first 13 days after weaning the addition of MSG to the diet increased daily food intake by proportionately 0·1 (P &lt; 0·01) as well as growth rate by proportionately 0·07 (P &lt; 0·01). Moreover, the addition of MSG to the diet was more effective with piglets of low weaning weight and thus contradicted the classical relationship between post-weaning performance and weaning weight. Finally, in an experiment where weaning occurred at lower ambient temperature, no improvement of post-weaning performance was observed following the addition of MSG.

Brain lesions and short-term endocrine effects of monosodium L-glutamate in goldfish, Carassius auratus.

Monosodium L-glutamate (MSG) was injected intraperitoneally into goldfish at a dosage of 2.5 mg/g body weight. At 24 h post-injection there was a marked hypertrophy and edema in the region of the nucleus lateralis tuberis (NLT) from the anterior margin of the pituitary stalk through to the posterior end of the NLT, irrespective of the sex of the goldfish. A similar hypertrophy and edema occurred ventral to the anterior commissure in the preoptic region in the anterior-ventral nucleus preopticus periventricularis (NPP). At 6 h post-injection a slight vacuolization was evident in these two regions, and at two days the hypertrophy and edema had abated from the extent observed at 24 h post-injection. At five and eight days post-injection only necrotic cells were found in the affected NLT region, but only a small band of necrotic cells was evident in the anterior-ventral preoptic region. No other brain lesions were evident. Serum levels of gonadotropin (GtH) were increased at 6 h, 24 h, and two days after treatment with MSG, but were similar to control values at five, seven and eight days after MSG in male and female goldfish. Exocytosis of small dark secretory granules in gonadotrophs was evident at 24 h after MSG in a fish with a somewhat greater increase in serum GtH than usually found. The time course of increased serum GtH levels postinjection of MSG is consistent with the observed time course of hypertrophy and atrophy of NLT neurons; the increase in serum levels of GtH is interpreted to reflect a stimulation of release of GtH-releasing factor from neurons in the NLT. Electron microscope investigation indicates that prolactin cells have increased secretory and synthetic activity from 24 h through to seven days post-injection of MSG. The mechanism for stimulation of the prolactin cells by MSG is not known. No other changes in activity of adenohypophysial secretory cells were found.

Studies on brain lesions after administration of monosodium L-glutamate to mice. II. Absence of brain damage following administration of monosodium L-glutamate in the diet

The effects of monosodium L-glutamate (MSG) on the brain of mice were examined by light-microscopy under the intended conditions of use of this material. Basal diet containing 5, 10 or 15% w/w MSG was fed to pregnant, lactating and weaning mice and libitum, resulting in the ingestion of 14.0, 42.8 or 42.0 g/kg body wt. of MSG a day respectively. Mice at the same developmental stages were given the basal diet and 5% w/w MSG in aqueous solution ad libitum, the maximum ingestion of MSG being 16.9 31.4 and 26.8 g/kg body wt. a day respectively. Light-microscopy examination revealed no pathological changes in the hypothalamic arcuate nuclei (AN) of all treated mice, i.e. pregnant females and their fetuses, lactating females and their sucklings, and weanling mice. Pregnant females and their fetuses, and weanling mice, injected subcutaneously with either 5.0 or 4.0 g/kg body wt. of MSG, showed “Glu-type lesions” in the hypothalamus.

Learned taste aversions induced by high doses of monosodium L-glutamate

Learned taste aversions, as measured by increased time to complete 100 licks of a sweetened condensed milk solution, were demonstrated by laboratory rats 4 days after consumption of the milk solution paired with high oral doses of monosodium l-glutamate (MSG). The hesitancy of the rats to consume milk on the test session cannot be simply attributed to direct action of the drug on motivation (e.g., hunger) or to drug debilitation. MSG has been reported to occasionally cause aversive effects in humans (Chinese restaurant syndrome), and the present experiments demonstrate that the effects of MSG are aversive to laboratory rats as well.