Glutamate Supplementation Research Articles

Glutamate increases the lean percentage and intramuscular fat content and alters gut microbiota in Shaziling pigs

This study aimed to explore the effects of glutamate (Glu) supplementation on the growth performance, carcass traits, meat quality, composition of amino acids and fatty acids in the longissimus dorsi muscle, and the colonic microbial community of Shaziling pigs. A total of 48 healthy male Shaziling pigs (150 d, 31.56 ± 0.95 kg) were randomly assigned to two groups, and fed a basal diet with no supplement (control group) or supplemented with 1% Glu (Glu group) for 51 d, and 6 pigs per group were finally slaughtered. Glu significantly increased the average daily gain (P = 0.039), lean percentage (P = 0.023), and intramuscular fat (IMF) content (P = 0.015), and decreased the fat percentage (P = 0.021) of Shaziling pigs. In the muscle, Glu increased the concentrations of inosine-5’-monophosphate (P = 0.094), Fe (P = 0.002), Cu (P = 0.052), and monounsaturated fatty acids (MUFAs) (P = 0.024), and decreased the content of C18:2n6 (P = 0.011), n6 polyunsaturated fatty acids (n6 PUFAs) (P = 0.014), and PUFAs (P = 0.014). Moreover, Glu significantly upregulated the mRNA expression of adipogenesis-related genes (FAS, SREBP-1C) (P = 0.032, P = 0.026) and muscle growth-related genes (MyHCⅡb, MyHCⅡx) (P = 0.038, P = 0.019) in the muscle, and increased the relative abundance of Spirochaetota (P < 0.001) and the acetic acid content in the colon (P = 0.039). Correlation analysis indicated that the acetic acid content was positively correlated with the relative Spirochaetota abundance and the IMF content, and a negative trend with the fat percentage of Shaziling pigs. In conclusion, these results indicated that Glu could simultaneously increase the lean percentage and IMF content and decrease the fat percentage of Shaziling pigs, and these beneficial effects may be related to increased colonic Spirochaetota abundance and acetic acid concentrations.

Dietary supplementation with glutamate enhanced antioxidant capacity, ammonia detoxification and ion regulation ability in Nile tilapia (Oreochromis niloticus) exposed to acute alkalinity stress

Saline-alkali aquaculture is an important way to improve the comprehensive utilization capacity of alkaline water and alleviate the fresh water crisis. This study investigated the effects of dietary L-glutamate (Glu) on ion regulation, ammonia detoxification and antioxidant capacity in Nile tilapia (Oreochromis niloticus) exposed to acute carbonate alkalinity stress. A total of 270 fish (6.06 ± 0.12 g) were fed three different dietary Glu supplements 0%, 1.5%, and 3.0% for 45 days. After the feeding trial, the fish were exposed to fresh water (control) or 53.57 mmol/l carbonate alkaline water for 24 h. The results showed that dietary Glu not only improved the weight gain and condition factors of tilapia but also promoted three reactions in which ammonia was converted into nontoxic substrates. After 24 h of alkalinity stress, tilapia fed a 15 g/kg Glu-supplement diet had considerably higher ion transport capacity in their gills compared to the control group (p < 0.05). Moreover, the gill structure of tilapia in the 15 g/kg Glu-supplement group was intact, while the structures in the other groups were impaired. Dietary Glu supplementation (15 g/kg) significantly increased the expression of genes related to urea and glutamine (Gln) synthesis. Additionally, the ammonia excretion capacity and antioxidant capacity were greatest in tilapia in the 15 g/kg Glu-supplement group (p < 0.05). These results indicated that in addition to promoting the growth of Nile tilapia, dietary Glu supplementation ameliorate the alkalinity tolerance of Nile tilapia and prevent oxidative damage, ionic toxicity and ammonia poisoning caused by acute carbonate alkalinity stress.

Effect of monosodium glutamate supplementation in diet on fatty acid profiles, genes expression related to lipid metabolism and egg yolk cholesterol in late phase of production in laying hens.

In an experiment with four treatments and five replicates, the effects of adding monosodium glutamate (MSG) to the diet in late phase of egg production was studied on performance, and lipid metabolism in laying hens. Dietary treatments included the control basal diet without MSG and the other treatments adding 0.4%, 0.8% and 1.2% MSG in the control diet respectively. The effect of supplementation of MSG on egg weight, egg production, feed conversion ratio and egg mass was insignificant (p < 0.05). Adding MSG to the diet significantly increased feed intake and blood polyunsaturated fatty acids concentration (p < 0.05). Intake of 0.8% and 1.2% MSG in the diet up regulated the mRNA expression of acetyl-coenzyme A carboxylase, fatty acid synthaseand lipoprotein lipase in the abdominal and liver tissues in comparison to the control group. Blood very low-density lipoprotein-cholesterol, triglyceridesand cholesterol concentration were increased in treatment fed with a diet containing 0.8% MSG compared to the control group (p < 0.05). The effect of MSG on total egg yolk cholesterol concentration was not significant. In conclusion, the results of the present experiment indicated that adding MSG increased feed intake and blood polyunsaturated fatty acid concentration.

Pyroptotic macrophages induce disruption of glutamate metabolism in periodontal ligament stem cells contributing to their compromised osteogenic potential.

Macrophage pyroptosis is of key importance to host defence against pathogen infections and may participate in the progression and recovery of periodontitis. However, the role of pyroptotic macrophages in regulating periodontal ligament stem cells (PDLSCs), the main cell source for periodontium renewal, remains unclear. First, we found that macrophage pyroptosis were enriched in gingiva tissues from periodontitis patients compared with those of healthy people through immunofluorescence. Then the effects of pyroptotic macrophages on the PDLSC osteogenic differentiation were investigated in a conditioned medium (CM)-based coculture system in vitro. CM derived from pyroptotic macrophages inhibited the osteogenic differentiation-related gene and protein levels, ALP activity and mineralized nodule formation of PDLSCs. The osteogenic inhibition of CM was alleviated when pyroptosis was inhibited by VX765. Further, untargeted metabolomics showed that glutamate limitation may be the underlying mechanism. However, exogenous glutamate supplementation aggravated the CM-inhibited osteogenic differentiation of PDLSCs. Moreover, CM increased extracellular glutamate and decreased intracellular glutamate levels of PDLSCs, and enhanced the gene and protein expression levels of system xc - (a cystine/glutamate antiporter). After adding cystine to CM-based incubation, the compromised osteogenic potency of PDLSCs was rescued. Our data suggest that macrophage pyroptosis is related to the inflammatory lesions of periodontitis. Either pharmacological inhibition of macrophage pyroptosis or nutritional supplements to PDLSCs, can rescue the compromised osteogenic potency caused by pyroptotic macrophages.

Glutamate rescues heat stress-induced apoptosis of Sertoli cells by enhancing the activity of antioxidant enzymes and activating the Trx1-Akt pathway in vitro

Heat stress reduces the number of Sertoli cells, which is closely related to an imbalanced redox status. Glutamate functions to maintain the equilibrium of redox homeostasis. However, the role of glutamate in heat treated Sertoli cells remains unclear. Herein, Sertoli cells from 3-week-old piglets were treated at 44 °C for 30 min (heat stress). Glutamate levels increased significantly following heat stress treatment, followed by a gradual decrease during recovery, while glutathione (GSH) showed a gradual increase. The addition of exogenous glutamate (700 μM) to Sertoli cells before heat stress significantly reduced the heat stress-induced apoptosis rate, mediated by enhanced levels of antioxidant substances (superoxide dismutase (SOD), total antioxidant capacity (TAC), and GSH) and reduced levels of oxidative substances (reactive oxygen species (ROS) and malondialdehyde (MDA)). Glutamate addition to Sertoli cells before heat stress upregulated the levels of glutamate-cysteine ligase, modifier subunit (Gclm), glutathione synthetase (Gss), thioredoxin (Trx1) and B-cell leukemia/lymphoma 2 (Bcl-2), and the ratio of phosphorylated Akt (protein kinase B)/total Akt. However, it decreased the levels of Bcl2-associated X protein (Bax) and cleaved-caspase 3. Addition of the inhibitor of glutaminase (Gls1), Bptes (Bis-2-(5-phenylacetamido-1,3,4-thiadiazol-2-yl)ethyl sulfide, 30 μM)to Sertoli cells before heat stress reversed these effects. These results inferred that glutamate rescued heat stress-induced apoptosis in Sertoli cells by enhancing activity of antioxidant enzymes and activating the Trx1-Akt pathway. Thus, glutamate supplementation might represent a novel strategy to alleviate the negative effect of heat stress.

Glucose-derived glutamate drives neuronal terminal differentiation in vitro

Neuronal maturation is the phase during which neurons acquire their final characteristics in terms of morphology, electrical activity, and metabolism. However, little is known about the metabolic pathways governing neuronal maturation. Here, we investigate the contribution of the main metabolic pathways, namely glucose, glutamine, and fatty acid oxidation, during the maturation of primary rat hippocampal neurons. Blunting glucose oxidation through the genetic and chemical inhibition of the mitochondrial pyruvate transporter reveals that this protein is critical for the production of glutamate, which is required for neuronal arborization, proper dendritic elongation, and spine formation. Glutamate supplementation in the early phase of differentiation restores morphological defects and synaptic function in mitochondrial pyruvate transporter-inhibited cells. Furthermore, the selective activation of metabotropic glutamate receptors restores the impairment of neuronal differentiation due to the reduced generation of glucose-derived glutamate and rescues synaptic local translation. Fatty acid oxidation does not impact neuronal maturation. Whereas glutamine metabolism is important for mitochondria, it is not for endogenous glutamate production. Our results provide insights into the role of glucose-derived glutamate as a key player in neuronal terminal differentiation.

Effect of Glutamate Supplementation in Broiler Chicken Feed to The Quality of Carcass

: Glutamate is an alternative feed additive that is safe and environmentally friendly in improving the quality of broiler chicken carcass. This study aims to determine the effect of glutamate produced by Lactobacilus plantarum MV on the quality of broiler chicken carcass. The aim of this research was to get the optimum doses of glutamate in feed broiler for increasing the quality of carcass. The design used was a Completely Randomized Design (CRD), with 6 treatments and 4 replications. This study used 240 broiler chicken strain MB 202 from PT Charoen Phokphand Indonesia, 1 day old and the treatment started at 7 days of age with 5 weeks of treatment. Each experimental unit consisted of 10 chickens. The Glutamate doses in groups were, A (0.4% commercial glutamate; B (0% glutamate); C (0.2% glutamate); D (0.4% glutamate); E (0.6% glutamate); F (0.8% glutamate). The results indicated that glutamate up to 0.8% had significant effects on carcass quality, consisting of reducing abdominal fat (0,64%) and cholesterol (0,64%), as well as increasing meat protein (73,09%) and cooking losses (26.69%). It can be concluded that 0,8% glutamate in broiler feed was increasing the quality of carcass.

Characterizing the effect of sodium reduction and monosodium glutamate supplementation on white and multigrain breads.

Sodium overconsumption has become a serious health concern resulting in the Food and Drug Administration (FDA) publishing voluntary sodium reduction guidelines for a wide spectrum of packaged and processed foods. Reducing sodium through the removal of salt may decrease the palatability of foods, thus increasing the need for new approaches to prevent such palatability loss. The objective of this research was to characterize white and multigrain breads with either 43% or 60% reduction in sodium and with and without monosodium glutamate (MSG) using descriptive analysis methodology as well as to identify the drivers of liking for white and multigrain breads of varying sodium contents with and without MSG. Significant differences were identified in the attributes of salty taste and aftertaste, savory aftertaste, and chewy and firm textures in white bread and of salty taste and aftertaste, sweet taste, and density in multigrain bread. By regressing consumer test data of these breads onto their principal component analysis biplots, textural attributes and salty taste and aftertaste were identified as primary drivers of liking in white and multigrain breads. Flavor enhancers such as MSG show promise in mitigating palatability loss that occurs when the sodium content of bread is greatly reduced and thus provide a promising solution to produce breads with an improved nutritional profile. Future research on flavor enhancement in other food matrices would be valuable as well as in other bread and carbohydrate-based food categories. PRACTICAL APPLICATION: The findings of our study suggest that texture and a salty taste and aftertaste drive consumer liking of reduced-sodium white and multigrain breads and liking of breads could be improved with the addition of monosodium glutamate. Increasing the acceptance of reduced-sodium food products could help to improve the health of the American population by resulting in a reduced risk of hypertension and subsequently heart attacks and stroke.

A Non-functional γ-Aminobutyric Acid Shunt Pathway in Cyanobacterium Synechocystis sp. PCC 6803 Enhances δ-Aminolevulinic Acid Accumulation under Modified Nutrient Conditions.

To redirect carbon flux from the γ-aminobutyric acid (GABA) shunt to the δ-aminolevulinic acid (ALA) biosynthetic pathway, we disrupted the GABA shunt route of the model cyanobacterium Synechocystis sp. PCC 6803 by inactivating Gdc, the gene-encoding glutamate decarboxylase. The generated ΔGdc strain exhibited lower intracellular GABA and higher ALA levels than the wild-type (WT) one. The ΔGdc strain’s ALA levels were ~2.8 times higher than those of the WT one when grown with levulinic acid (LA), a competitive inhibitor of porphobilinogen synthase. Abiotic stress conditions including salinity induced by 10 mM NaCl and cold at 4 °C increased the ALA levels in ΔGdc up to ~2.5 and 5 ng g−1 cell DW, respectively. The highest ALA production in the ΔGdc cyanobacteria grown in BG11 medium was triggered by glucose induction, followed by glutamate supplementation with 60 mM of LA, thereby resulting in ~360 ng g−1 cell DW of ALA, that is >300-fold higher ALA accumulation than that observed in ΔGdc cyanobacteria grown in normal medium. Increased levels of the gdhA (involved in the interconversion of α-ketoglutarate to glutamate) and the hemA (a major regulatory target of the ALA biosynthetic pathway) transcripts occurred in ΔGdc cyanobacteria grown under modified growth conditions. Our study provides critical insight into the facilitation of ALA production in cyanobacteria.

Sustainable citric acid production from CO2 in an engineered cyanobacterium.

Citric acid is one of the most widely used organic acids in the world, with applications ranging from acidity regulation in food and beverages to metal chelation in hydrometallurgical processes. Most of its production is currently derived from fermentative processes, using plant-derived carbon feedstocks. While these are currently dominant, there is an increasing need to develop closed-loop production systems that reduce process carbon footprint. In this work, we demonstrate for the first time that an engineered marine cyanobacterium Synechococcus sp. PCC 7002 can be used as a sustainable chassis for the photosynthetic conversion of CO2 to citric acid. Decreased citric acid cycle flux, through the use of a theophylline-responsive riboswitch, was combined with improved flux through citrate synthase and enhanced citric acid excretion, resulting in a significant improvement to citric acid production. While allowing citrate production, this strategy induces a growth defect which can be overcome by glutamate supplementation or by fine-tuning aconitase levels, resulting in an increase in production relative to WT of over 100-fold. This work represents a first step toward sustainable production of a commodity organic acid from CO2.

Goats as Valuable Animal Model to Test the Targeted Glutamate Supplementation upon Antral Follicle Number, Ovulation Rate, and LH-Pulsatility.

Simple SummaryExogenous glutamate administration to yearling-anestrous goats enhanced not only ovarian function (i.e., ovulation rate and antral follicle number) but also denoted undoubted effects at the hypothalamic-pituitary level, augmenting LH pulsatility. Our results show not only the use of glutamate as a clean alternative but also as an interesting reproductive strategy to amplify ovarian function, considering goats as an animal model. While this should enlarge the possibility of escalating our knowledge regarding the hypothalamic-pituitary-gonadal modulation by glutamate, such research outcomes may also embrace potential translational implications.The potential effect of intravenous administration of glutamate on the ovarian activity and the LH secretion pattern, considering the anestrous yearling goat as an animal model, were assessed. In late April, yearling goats (n = 20) were randomly assigned to either (1) Glutamate supplemented (GLUT; n = 10, Live Weight (LW) = 29.6 ± 1.02 kg, Body Condition (BCS) = 3.4 ± 0.2 units; i.v. supplemented with 7 mg GLUT kg−1 LW) or (2) Non-supplemented (CONT; n = 10; LW = 29.2 ± 1.07 kg, BCS = 3.5 ± 0.2 units; i.v. saline). The oats were estrus-synchronized; blood sampling (6 h × 15 min) was carried out for LH quantification. Response variables included pulsatility (PULSE), time to first pulse (TTFP), amplitude (AMPL), nadir (NAD), and area under the curve (AUC) of LH. Ovaries were ultra-sonographically scanned to assess ovulation rate (OR), number of antral follicles (AF), and total ovarian activity (TOA = OR + AF). LH-PULSE was quantified with the Munro algorithm; significant treatment x time interactions were evaluated across time. The variables LW and BCS did not differ (p > 0.05) between the experimental groups. Nevertheless, OR (1.77 vs. 0.87 ± 0.20 units), TOA (4.11 vs. 1.87 ± 0.47 units) and LH-PULSE (5.0 vs. 2.2 pulses 6 h-1) favored (p < 0.05) to the GLUT group. Our results reveal that targeted glutamate supplementation, the main central nervous system neurotransmitter, arose as an interesting strategy to enhance the hypothalamic–hypophyseal–ovarian response considering the anestrous-yearling goat as an animal model, with thought-provoking while promising translational applications.

Glutamate Supplementation Improves Growth Performance, Rumen Fermentation, and Serum Metabolites in Heat-Stressed Hu Sheep.

This study evaluated the effect of glutamate supplementation on the physiological parameters of heat-stressed Hu sheep. Forty-eight male Hu sheep with an average initial body weight of 17.74 ± 0.17 kg were randomly divided into two groups: The control group (CON) was fed a basal diet and a treatment group (GLU) was fed a basal diet + 3 g/head/day of L-glutamate. There were six replications in each group with four sheep in each replication for a 90 days feeding test. Growth performance, serum biochemistry, and serum hormones were measured during phase 1 (1–30 days), phase 2 (31–60 days), and phase 3 (61–90 days) of the experiment; rumen fermentation characteristics, nutrient digestibility, and slaughter performance were measured at the end of the experimental periods. There were no differences in growth performance, serum biochemical indices, and immune indices between CON and GLU during phases 1 and 2. However, a higher average daily gain (ADG), a lower average daily feed intake (ADFI), and a lower F:G ratio (ADFI/ADG) were observed in GLU during phase 3 (p < 0.05). Serum levels of glutamate, globulin, immunoglobulin A, immunoglobulin G, immunoglobulin M, and growth hormone in GLU were higher than those in CON only on day 90 (p < 0.05). Serum levels of heat shock protein 70, adrenocorticotrophic hormone, corticosterone, triiodothyronine, and tetraiodothyronine in GLU were lower than those in CON on day 90 (p < 0.05). At the end of the experiment, ruminal pH, microbial crude protein, ammonia nitrogen, and isovalerate concentrations in GLU were higher than those in CON (p < 0.05). The apparent digestibility of dry matter, organic matter, and crude protein in GLU was higher than those in CON (p < 0.05). There were no differences in carcass traits and organ indices but spleen weight and spleen index tended to be higher in GLU. In conclusion, dietary glutamate supplementation improved rumen fermentation, increased nutrition digestibility and metabolism, enhanced immunity, and promoted growth performance of heat-stressed Hu sheep. This suggests that a longer period of glutamate supplementation (not less than 60 days) at a level of 3 g/head/day is beneficial to Hu sheep under heat stress.

System Xc− inhibition blocks bone marrow-multiple myeloma exosomal crosstalk, thereby countering bortezomib resistance

Multiple myeloma (MM) cells derive proliferative signals from the bone marrow (BM) microenvironment via exosomal crosstalk. Therapeutic strategies targeting this crosstalk are still lacking. Bortezomib resistance in MM cells is linked to elevated expression of xCT (the subunit of system Xc−). Extracellular glutamate released by system Xc− can bind to glutamate metabotropic receptor (GRM) 3, thereby upregulating Rab27-dependent vesicular trafficking. Since Rab27 is also involved in exosome biogenesis, we aimed to investigate the role of system Xc− in exosomal communication between BM stromal cells (BMSCs) and MM cells. We observed that expression of xCT and GRMs was increased after bortezomib treatment in both BMSCs and MM cells. Secretion of glutamate and exosomes was simultaneously enhanced which could be countered by inhibition of system Xc− or GRMs. Moreover, glutamate supplementation increased exosome secretion by increasing expression of Alix, TSG101, Rab27a/b and VAMP7. Importantly, the system Xc− inhibitor sulfasalazine reduced BMSC-induced resistance to bortezomib in MM cells in vitro and enhanced its anti-MM effects in vivo. These findings suggest that system Xc− plays an important role within the BM and could be a potential target in MM.

Glutamate attenuates lipopolysaccharide induced intestinal barrier injury by regulating corticotropin-releasing factor pathway in weaned pigs.

ObjectiveThe purpose of this study was to evaluate the protection of glutamate (GLU) against the impairment in intestinal barrier function induced by lipopolysaccharide (LPS) stress in weaned pigs.MethodsTwenty-four weaned pigs were divided into four treatments containing: i) non-challenged control, ii) LPS-challenged control, iii) LPS+1.0% GLU, and iv) LPS+2.0% GLU. On day 28, pigs were treated with LPS or saline. Blood samples were collected at 0, 2, and 4 h post-injection. After blood samples collection at 4 h, all pigs were slaughtered, and spleen, mesenteric lymph nodes, liver and intestinal samples were obtained.ResultsDietary GLU supplementation inhibited the LPS-induced oxidative stress in pigs, as demonstrated by reduced malondialdehyde level and increased glutathione level in jejunum. Diets supplemented with GLU enhanced villus height, villus height/crypt depth and claudin-1 expression, attenuated intestinal histology and ultrastructure impairment induced by LPS. Moreover, GLU supplementation reversed intestinal intraepithelial lymphocyte number decrease and mast cell number increase induced by LPS stress. GLU reduced serum cortisol concentration at 4 h after LPS stress and downregulated the mRNA expression of intestinal corticotropin-releasing factor signal (corticotrophin-releasing factor [CRF], CRF receptor 1 [CRFR1], glucocorticoid receptor, tryptase, nerve growth factor, tyrosine kinase receptor A), and prevented mast cell activation. GLU upregulated the mRNA expression of intestinal transforming growth factor β.ConclusionThese findings indicate that GLU attenuates LPS-induced intestinal mucosal barrier injury, which is associated with modulating CRF signaling pathway.

Effects of rumen-protected glutamate supplementation during the periparturient period on digestibility, inflammation, metabolic responses, and performance in dairy cows

The objective of this study was to evaluate the effects of feeding rumen-protected glutamate during the periparturient period (d -21 ± 3 to d 21 ± 3 relative to calving) on apparent total-tract digestibility (ATTD), inflammation, metabolic responses, and production performance of dairy cows. Fifty-two multiparous Holstein cows were blocked by parity, body condition score, and expected calving date, and randomly assigned to one of the experimental diets with rumen-protected monosodium glutamate (RP-Glu; intestinally available Glu = 8.8%) or without RP-Glu (control) at d -21 ± 3 relative to expected calving date. The RP-Glu was fed at 4% and 3% of dietary dry matter, before and after calving, respectively. Prepartum diets contained 17.1% and 16.5% crude protein, and 13.1% and 13.3% starch, and postpartum diets contained 18.8% and 18.3% crude protein, and 22.5% and 22.7% starch on a dry matter basis, respectively for RP-Glu and control treatments. A subset of 19 cows was used to measure ATTD. Cows fed the RP-Glu had greater ATTD of dry matter (70.6 vs. 69.1%), crude protein (75.1 vs. 72.6%), and ether extract (66.0 vs 61.2%) on d 5 ± 1 after calving. Cows fed the RP-Glu also had greater dry matter intake (15.7 vs. 13.7 kg/d) on d 1 after calving. Cows fed the RP-Glu had greater plasma concentrations of Glu (4.60 vs. 3.89 µmol/dL) and insulin-like growth factor-1 (44.2 vs. 30.1 mg/mL), lower serum concentrations of free fatty acids (670 vs. 981 μEq/L) and total bilirubin (0.22 vs. 0.34 mg/dL), and lower plasma 3-methylhistidine concentration (1.28 vs. 1.50 μmol/dL) on d 4 after calving. However, these treatment effects observed between d 1 and d 5 ± 1 immediately after calving did not continue until d 21 after calving. Concentrations of serum amyloid A, serum haptoglobin, and plasma lipopolysaccharide binding protein were not affected by the treatment. In addition, no differences were observed for serum β-hydroxybutyrate concentration and milk yield during the postpartum period between the 2 groups, and cows fed the RP-Glu had a decreased lactose yield. These findings suggest that feeding RP-Glu during the periparturient period can increase digestive capacity and feed intake, and decrease mobilization of body fat and protein immediately after calving without increasing milk production.

Tillering response of liquid organic fertilizer and monosodium glutamate supplementation on Ganyong (Canna discolor Lindl.)

Ganyong (Canna discolor) is a plant that contains a high carbohydrate content, utilizing as alternative food for rice, especially in Indonesia. One of the factors affecting growth is the quantity of tillers, which affect the productivity of Ganyong's tuber. The purpose of this study was to discover the optimal combination of liquid organic fertilizer and monosodium glutamate to enhance the number of tillers. This study employed a randomized complete block design with a two-factor structure. The first factor to consider was the concentration of liquid organic fertilizer, which was specified as 0 ml/L, 2 ml/L, 3 ml/L, and 4 ml/L. The second factor was the monosodium glutamate dosage, which ranged from 0 to 3 g/plant, 6 g/plant, and 9 g/plant. Ganyong were cultivated for six months on farmland at an elevation of 460 m asl. Supplementation with liquid organic fertilizer resulted in a significant increase in the number of tillers. While monosodium glutamate supplementation had no significant effect on the formation of tillers. Combining liquid organic fertilizer at a concentration of 3 ml/L with monosodium glutamate 6 g/plant resulted in the optimal number of tillers.

Proteomic Analysis and Promoter Modification of Bacillus thuringiensis to Improve Insecticidal Vip3A Protein Production.

Insecticidal protein Vip3A secreted from B. thuringiensis is a potential biocontrol agent for control of lepidopteran pests. Under laboratory conditions, high albeit variable Vip3A production from the local isolate Bt294 was only obtained from a much enriched TB culture medium. Proteomic analysis and strain improvement were therefore performed to improve Vip3A production. Studies indicated that the buffer capacity, carbon source, and nitrogen source are critical to efficiently produce Vip3A. Medium with lower amounts of peptone and yeast extract (compared to TB), with an additional carbon source and phosphate buffer (LB*G medium) was found to give reasonable yields of Vip3A. Proteomic analysis revealed higher expression of proteins involved in glutamate and histidine biosynthesis in cells cultured in TB compared to LB about 58 and 33 times, respectively. Experiments confirmed that glutamate supplementation could increase Vip3A production. In addition, promoter substitution with that of cry3A increased Vip3A yields by about 20-30%. Overall, very high yields of Vip3A could be obtained by culturing Bt294 (Pcry3A-vip3Aa64) in LB*G medium with glutamate supplementation.

TFEB Supports Pancreatic Cancer Growth through the Transcriptional Regulation of Glutaminase.

Simple SummaryPancreatic cancer is a highly lethal tumor with poor prognosis. In general, pancreatic cancer is not detected in its early stages since there are no signs or symptoms. A surgical resection gives the best chance for a cure, but these lesions are detected at the terminal or metastatic stages in most patients and surgery is therefore no longer feasible. New therapeutic options are thus necessary for the pancreatic cancer treatment. Alterations to metabolic pathways have recently attracted great interest as possible cancer treatments and many studies have reported that targeting glutaminase is an ideal approach in many cancers. Here, we provide reliable evidence that pancreatic cancer requires TFEB for maintaining glutaminase-mediated glutamine metabolism, and that this is an attractive new target for pancreatic cancer therapy.Transcription factor EB (TFEB) is a master regulator of lysosomal function and autophagy. In addition, TFEB has various physiological roles such as nutrient sensing, cellular stress responses, and immune responses. However, the precise roles of TFEB in pancreatic cancer growth remain unclear. Here, we show that pancreatic cancer cells exhibit a significantly elevated TFEB expression compared with normal tissue samples and that the genetic inhibition of TFEB results in a significant inhibition in both glutamine and mitochondrial metabolism, which in turn suppresses the PDAC growth both in vitro and in vivo. High basal levels of autophagy are critical for pancreatic cancer growth. The TFEB knockdown had no significant effect on the autophagic flux under normal conditions but interestingly caused a profound reduction in glutaminase (GLS) transcription, leading to an inhibition of glutamine metabolism. We observed that the direct binding of TFEB to the GLS and TFEB gene promotors regulates the transcription of GLS. We also found that the glutamate supplementation leads to a significant recovery of the PDAC growth that had been reduced by a TFEB knockdown. Taken together, our current data demonstrate that TFEB supports the PDAC cell growth by regulating glutaminase-mediated glutamine metabolism.

Dietary monosodium glutamate supplementation during the feed training of pacamã (Lophiosilurus alexandri): Growth performance and intestinal histomorphometry

Feed training of carnivorous fish is a delicate and stressful process. Thus, feed additives that reduce stress and encourage fish consumption could improve training efficiency. Therefore, the aim of this study was to evaluate monosodium glutamate (MSG) dietary supplementation during pacamã (Lophiosilurus alexandri) feed training through growth performance and intestinal histomorphometry. Fish were trained by the method of gradual diet transition, using five diets with increasing proportions of commercial diet and decreasing proportions of gelatin. A quadruplicate experimental design was performed with seven treatments, consisted in diets supplemented with different levels of MSG (0.0; 2.0; 8.0; 16.0; 29.0; 34.0 and 42.0 g/kg). Pacamã (0.17 ± 0.01 g) were distributed in 28 tanks (30 fish per tank) and trained for 41 days with the experimental diets. There were no effects (p > .05) of MSG on growth performance and feed training indices. However, fish trained with diets supplemented with 42.0 g/kg of MSG presented higher number of goblet cells in the anterior portion of intestine (p < .05). These results demonstrate that MSG did not act on growth performance and feed training efficiency of pacamã, and high levels of MSG can cause dietary stress on fish intestinal mucosa.

Role of the Outer Inflammatory Protein A/Cystine–Glutamate Transporter Pathway in Gastric Mucosal Injury Induced by Helicobacter pylori

INTRODUCTION:Helicobacter pylori infection is a major cause of gastrointestinal diseases. However, the pathogenesis of gastric mucosal injury by H. pylori remains unclear. Exogenous glutamate supplementation protects against gastric mucosal injury caused by H. pylori. Previously, we showed that aspirin-induced gastric injury is associated with reduction in glutamate release by inhibition of cystine–glutamate transporter (xCT) activity. We hypothesized that the xCT pathway is involved in H. pylori-induced gastric mucosal injury. In this study, we tested the activity of xCT and evaluated the regulatory effect of outer inflammatory protein (Oip) A on xCT in H. pylori-induced gastric mucosal injury.METHODS:In the H. pylori-infected mice and cell lines, the activity of xCT and the regulatory effect of microRNA on xCT were tested, and the effect of OipA from H. pylori on xCT activity was observed.RESULTS:The results of in vivo and in vitro experiments showed that H. pylori infection induced gastric mucosal injury. This was accompanied by a reduction in xCT activity, which was attenuated by exogenous glutamate treatment. Furthermore, the expression of miR-30b was upregulated, and miR-30b inhibitors significantly restored xCT activity and gastric mucosal injury caused by H. pylori infection. The OipA, a virulence protein from H. pylori, significantly upregulated the expression levels of miR-30b and inhibited xCT activity.DISCUSSION:OipA plays a significant role in H. pylori-induced gastric mucosal injury, and the effects are mediated by micro30b/xCT pathway.