MSG-induced Obesity Research Articles

The M 1 -muscarinic acetylcholine receptor subtype may play a role in learning and memory performance in the hippocampus of neonatal monosodium glutamate-obese rats.

Here, we investigate the effects of obesity induced by monosodium glutamate (MSG) on cognitive impairment and whether this model induces any alteration in the affinity, density, and subtypes of muscarinic acetylcholine receptors (mAChRs) in rat hippocampus. Healthy rats were used as controls, and MSG-obese rats were selected via the Lee index > 0.300. The effects of MSG-induced obesity on hippocampal spatial learning and memory processes were evaluated by using the working memory versions of the Morris' water maze task and the evaluation of mAChRs by binding assay and their subtypes by immunoprecipitation assays. [ 3 H]Quinuclidinyl benzilate specific binding analysis showed that the equilibrium dissociation constant (K D ) did not differ between control and MSG, indicating that affinity is not affected by obesity induced by MSG. The maximum number of binding sites (B max ) obtained in MSG subjects was lower than that obtained from control rats, indicating a decrease in the expression of total mAChRs. Immunoprecipitation assays reveal a decrease in the expression of M 1 subtype of MSG when compared with control rats (M 2 to M 5 subtypes did not differ between control and MSG). We also observed that MSG promotes a disruption of the spatial working memory which was accompanied by a decrease in the M 1 mAChR subtype in rat hippocampus, thus suggesting deleterious long-term effects besides the obesity. In conclusion, these findings provide new insights into how obesity can influence spatial learning and memory that is hippocampal-dependent. The data suggest that the M 1 mAChR subtype protein expression is a potential therapeutic target.

An Early and Sustained Inflammatory State Induces Muscle Changes and Establishes Obesogenic Characteristics in Wistar Rats Exposed to the MSG-Induced Obesity Model.

The model of obesity induced by monosodium glutamate cytotoxicity on the hypothalamic nuclei is widely used in the literature. However, MSG promotes persistent muscle changes and there is a significant lack of studies that seek to elucidate the mechanisms by which damage refractory to reversal is established. This study aimed to investigate the early and chronic effects of MSG induction of obesity upon systemic and muscular parameters of Wistar rats. The animals were exposed to MSG subcutaneously (4 mg·g-1 b.w.) or saline (1.25 mg·g-1 b.w.) daily from PND01 to PND05 (n = 24). Afterwards, in PND15, 12 animals were euthanized to determine the plasma and inflammatory profile and to assess muscle damage. In PND142, the remaining animals were euthanized, and samples for histological and biochemical analyses were obtained. Our results suggest that early exposure to MSG reduced growth, increased adiposity, and inducted hyperinsulinemia and a pro-inflammatory scenario. In adulthood, the following were observed: peripheral insulin resistance, increased fibrosis, oxidative distress, and a reduction in muscle mass, oxidative capacity, and neuromuscular junctions, increased fibrosis, and oxidative distress. Thus, we can conclude that the condition found in adult life and the difficulty restoring in the muscle profile is related to the metabolic damage established early on.

Multi-probiotic consumption sex-dependently interferes with MSG-induced obesity and concomitant phagocyte pro-inflammatory polarization in rats: Food for thought about personalized nutrition

Epidemic scope which obesity has reached in many countries necessitates shifting the emphasis in medicine from traditional reaction to individualized and personalized prevention. Numerous trials convincingly prove sexual dimorphism of obesity in morbidity, pathophysiology, comorbidity, outcomes and prophylaxis efficacy. Obesity is characterized by chronic systemic low-grade inflammation that creates the preconditions for the emergence of numerous comorbidities. Leading role in the initiation, propagation and resolution of inflammation belongs to tissue resident and circulating phagocytes. The outcome of inflammation largely depends on phagocyte functional polarization, which in turn is governed by environmental stimuli. Gut microbiota (GM), whose disturbances are one of the key pathogenetic features in obesity, substantially affect phagocyte functions and can either aggravate or calm obesity-associated inflammation. Probiotics possess promising physiological functions, including microbiota-restoring and anti-inflammatory traits, that may possibly help prevent obesity. However, sex-specific effects of probiotic supplementation for targeted obesity prevention remain unknown. The aim of the current study was aimed to compare the effect of multi-probiotic preparation used in prophylactic regimen on the adiposity, profile of culturable GM and its short-chain fatty acids as well as on functional profile of phagocytes from different locations in male and female rats with monosodium glutamate (MSG)-induced obesity. Obesity was induced by neonatal MSG injections in male and female rats, who were given the multi-species probiotic during juvenile and adult developmental stages. Culturable fecal and mucosa-associated microbiota of the intestine were examined using selective diagnostic media. Short-chain fatty acid profile in fecal samples was determined by GC-MS. Phagocyte functional profile was evaluated using flow cytometry and colorimetric methods. Probiotic supplementation after the administration of MSG prevented weight gain and fat accumulation, inflammatory phagocyte activation and alterations in GM in female rats. In male MSG-injected rats, probiotic supplementation restricted but did not prevent weight gain and fat deposition, alleviated but did not prevent systemic inflammation, prevented the alterations in GM, but with residual imbalance in the ratio of obligate anaerobic to facultative anaerobic bacteria. Our findings emphasize the necessity of sex-centered approaches to the prophylactic use of probiotics in obesity in the context of predictive preventive and personalized medicine.

Study on the effect of vitamin D on obesity and fatty liver induced by monosodium glutamate in male albino rats

Background One of the most common hepatic disorders is nonalcoholic fatty-liver disease. The best model used for nonalcoholic fatty-liver disease is the monosodium glutamate (MSG)-induced obesity. MSG is a common flavor enhancer used in different food products. Vitamin-D deficiency increased risks of obesity and nonalcoholic fatty-liver disease. However, much is still unknown about the link between vitamin D and nonalcoholic fatty-liver disease in obesity. Aim The aim was to investigate the effect of vitamin D on MSG-induced obesity and nonalcoholic fatty-liver disease in rats. Materials and methods Forty adult male albino rats were divided into four equal groups: control group, vitamin-D-treated group, MSG-treated group, MSG, and vitamin-D-treated group, at the end of the experimental period, blood samples were taken. Also, livers were dissected for histopathology. Results Vitamin D+MSG significantly decreased the body weight, serum levels of glucose, insulin and homeostasis model assessment-estimated insulin resistance, triglycerides, tumor necrosis factor-alpha, aspartate aminotransferase, alanine aminotransferase, and the liver malondialdehyde, while increased the liver glutathione levels and improved the liver histological findings compared with MSG group. Conclusion Vitamin D has a hepatoprotective effect on the MSG-induced obesity and nonalcoholic fatty-liver disease.

Prdm16-Mediated Browning is Involved in Resistance to Diet-Induced and Monosodium Glutamate-Induced Obesity.

PurposeTo investigate resistance to diet-induced obesity (DIO) and monosodium glutamate (MSG)-induced obesity as well as the underlying mechanisms.MethodsNewborn mice were used to construct DIO and MSG-induced obesity models. Obesity indices, such as body weight, body length, Lee index, body temperature, food intake, fat weight, and leptin level, were examined. Mice that did not exhibit obesity were defined as the obesity-resistant group. The morphological changes of white adipose tissue were observed by hematoxylin and eosin staining, and expression levels of PR domain containing 16 (Prdm16) and uncoupling protein-1 (Ucp-1) in white adipose tissue were measured by Western blot.ResultsObesity-resistant mice fed a high-fat diet showed resistance beginning at week 5 along with lower weights and lengths than those in the obesity group from weeks 5 to 12. MSG-induced obesity-resistant mice showed features consistent with resistance to obesity from week 1 along with higher body lengths relative to the obesity group; however, the weight difference was not significant until week 10, when body weights decreased significantly in obesity-resistant mice. The Lee index was lower in obesity-resistant mice than in the obesity group and the normal group, further suggesting obesity resistance. Additionally, obesity-resistant mice showed higher levels of leptin, whereas obese mice induced by a high-fat diet showed leptin resistance. Furthermore, Prdm16 and Ucp-1 levels were both downregulated in the obesity group and upregulated in obesity-resistant mice, showing that white fat browning was highest in obesity-resistant mice.ConclusionThe phenotypes of mice with DIO and MSG-induced obesity differed. Obesity resistance might be related to Prdm16 and Ucp-1-mediated white adipocyte browning.

Splenic participation in glycemic homeostasis in obese and non-obese male rats

We evaluated the effects of splenectomy on glucose homeostasis in obese and non-obese rats. Obesity was induced by subcutaneous injections of monosodium glutamate (MSG; 4g/kg) in neonatal rats. Control (non-obese) animals received equimolar saline. Splenectomy (SPL) was performed at 21 or 60 days of life (SPL21 and SPL60) in MSG obese and non-obese groups. Glucose tolerance, insulin resistance (IR), adiposity, histology of white adipose tissue (WAT) depots and glucose-induced insulin secretion (GIIS) in isolated pancreatic islets were evaluated at 90 days of life. In non-obese, despite of hyperphagia, the spleen ablation reduced body weight gain and energy efficiency, without changes in GIIS or IR. Slight reduction in glucose tolerance and augmented adipocyte size in subcutaneous WAT was noted in non-obese SPL21 group. In MSG-SPL21 rats was observed augmented body weight gain and energy efficiency, without alter adipocyte size. In contrast, MSG-SPL60 rats had lower body weight gain, reduced energy efficiency and smaller adipocyte size in WAT visceral depot in relation to MSG non-operated. Spleen ablation reduced insulin plasma levels in the MSG-SPL21 and MSG-SPL60 groups. Moreover, splenectomy reduced GIIS and improved glucose tolerance in MSG-SPL21 group. In MSG-SPL60 rats were observed reduction in IR, without changes in GIIS, despite of elevated glucokinase expression in pancreatic islets. In conclusion, spleen ablation reduces body weight in non-obese rats and slightly modifies glucose homeostasis. In contrast, in MSG-induced obesity, absence of the spleen can ameliorate glucose tolerance and reduce insulin secretion, improving insulin sensitivity.

Coicis Semen formula treating monosodium glutamate-induced obesity in mice by alleviating hypothalamic injury

ABSTRACT Obesity is a worldwide public health issue, however, efficient strategies to treat obesity without systemic damage is still in serious lack. Herein, we proved that a significant decrease in body weight and abdominal circumference was observed when monosodium glutamate (MSG)-induced obese mice were orally treated with Coicis Semen formula. Consistently, computed tomography and magnetic resonance imaging results showed that both whole-body fat content and subcutaneous fat thickness were lowered, which was further confirmed by hematoxylin–eosin staining. In addition, the weight ratios of adipose tissues and liver to the body weight were reduced, due to the decreased lipid accumulation. The increased triacylglycerol, total cholesterol, and inflammatory cytokines could also be downregulated after the treatment. Furthermore, the neuronal injury marker and inflammatory cytokines in the hypothalamus were obviously reduced after the treatment, revealing that the protective effect of Coicis Semen formula on MSG-induced obesity was achieved by alleviating hypothalamic injury.

Cortical tau burden and behavioural dysfunctions in mice exposed to monosodium glutamate in early life.

Although monosodium glutamate (MSG)-induced neurotoxicity has been recognized for decades, the potential similarities of the MSG model to Alzheimer’s disease (AD)-type neuropathology have only recently been investigated. MSG-treated mice were examined behaviourally and histologically in relation to some features of AD. Four-week old mice received 5 subcutaneous MSG (2 g/kg) injections on alternate days, or saline. At age 10–12 weeks, they were given a battery of behavioural tests for species-typical behaviours and working memory. The mice were killed at 12 weeks and the brains excised. Accumulation of hyperphosphorylated tau protein was assessed in cortical and hippocampal neurons by immunohistochemistry, and in cerebral cortical homogenates. A 78% increase in cortical concentrations of phosphorylated tau protein was observed in the MSG mice. Intracellular hyperphosphorylated tau immunostaining was observed diffusely in the cortex and hippocampus, together with cortical atrophic neurons, extensive vacuolation and dysmorphic neuropil suggestive of spongiform neurodegeneration. Nest-building was significantly impaired, and spontaneous T-maze alternation was reduced, suggesting defective short-term working memory. Subcutaneous MSG treatment also induced a 56% reduction in exploratory head dips in a holeboard (P = 0.009), and a non-significant tendency for decreased burrowing behaviour (P = 0.085). These effects occurred in the absence of MSG-induced obesity or gross locomotor deficits. The findings point to subcutaneous MSG administration in early life as a cause of tau pathology and compromised species-typical behaviour in rodents. Determining whether MSG can be useful in modelling AD requires further studies of longer duration and full behavioural characterization.

The effects of Z56822977 on biosynthesis of serotonin in the brain of rats in the conditions of MSG-induced obesity.

Wstęp: Badanie przeprowadzono w celu wyjaśnienia wpływu Z56822977 na biosyntezę serotoniny w mózgu szczurów z otyłością wy-wołaną podawaniem glutaminianu sodu (monosodium glutamate, MSG). Materiał i metody: W badaniu wykorzystano 18 samców szczura. Zwierzęta podzielono na trzy grupy: 1 - grupa kontrolna, 2 - grupa MSG, 3 - grupa MSG + Z56822977. Szczurzym oseskom w grupie 2 i 3 podawano podskórnie MSG rozpuszczony w soli fizjologicznej w dawce 4 mg/g masy ciała w objętości 8 μl/g w 2., 4., 6., 8. i 10. dniu życia. Grupie 3 podawano doustnie wodny roztwór Z56822977 w dawce 25 mg/kg w objętości 1 ml/kg. Pierwszą dawkę Z56822977 podawano po ukończeniu 4 tygodni życia, a następnie kontynuowa-no podawanie badanej substancji cyklicznie wedlug schematu tydzień podawania substancji badanej/3 tygodnie przerwy. Zwierzętom z grupy MSG podawano odpowiednio 1 ml/kg wody doustnie. Przez pierwsze 4 miesiące życia szczury otrzymywały standardową karmę. Zmierzono zawartość serotoniny, tryptofanu i 5-hydroksytryptofanu (5-HTr) oraz aktywność hydroksylazy tryptofanowej (tryptophan hydroxylase, TRH), dekarboksylazy aminokwasów (amino acid decarboxylase, AADC) i monoaminooksydazy (MAO) w tkance mózgowej. WYNIKI: Wykazano, że podawanie Z56822977 ma pozytywny wpływ na główne wskaźniki otyłości, co odzwierciedlają zmiany podsta-wowych parametrów fizjologicznych i biochemicznych [zmniejszenie masy ciała o 13% vs. MSG (p < 0,05); zmniejszenie wskaźnika masy ciała (body mass index, BMI), wskaźnika Lee oraz masy tkanki tłuszczowej trzewnej odpowiednio o 18%, 7% i 55%, (p < 0,05) w porównaniu z grupą MSG]. Zawartość tryptofanu i serotoniny była istotnie niższa (p < 0,05) u szczurów z otyłością wywołaną przez MSG. W badaniach wykazano, że u otyłych szczurów aktywność MAO zwiększa się o 97% (p < 0,05), a aktywność TRH i AADC odpowiednio o 44% i 53% (p < 0,05). Podawanie Z56822977 powodowało zwiększenie zawartości serotoniny i tryptofanu w mózgach szczurów i przywracało poziom aktywności enzymów (MAO, TRH, AADC) do wartości mierzonych u zwierząt kontrolnych. WNIOSKI: Wiadomo, że otyłość wiąże się z zaburzeniem syntezy serotoniny w mózgu szczurów. Jednak podawanie Z56822977 prowadzi do normalizacji stężenia serotoniny i tryptofanu oraz przywrócenia prawidłowej aktywności enzymów uczestniczących w biosynte-zie i degradacji serotoniny. Podawanie Z56822977, cząsteczki wpływającej na układ serotoninergiczny, może powodować korzystne efekty w leczeniu otyłości wywołanej przez MSG u szczurów. Można rozważać zastosowanie cząsteczki Z56822977 jako nowego leku stosowanego w otyłości, jednak konieczne są dalsze badania w celu potwierdzenia jej działania.

The correction of the metabolic parameters of msg-induced obesity in rats by 2-[4-(benzyloxy) phenoxy] acetic acid

Epidemiological data showed that the number of obese people increases swiftly in all countries. Obesity can evoke metabolic syndrome or second type diabetes (T2D). So, the aim of our study was to investigate the influence of 2-[4-(benzyloxy) phenoxy] acetic acid on metabolic parameters of monosodium glutamate (MSG)-induced obesity in rats. We divided the rats as follows: 1- control group, 2 - MSG-group, 3 - MSG + 2-[4-(benzyloxy) phenoxy] acetic acid group. We investigated anthropometric parameters and blood biochemistry. It was established that MSG induced the development of visceral obesity in rats, in particular, it increased the Lee index, body mass index, deposits of subcutaneous, gonadal and visceral adipose tissue. The administration of 2-[4-(benzyloxy) phenoxy] acetic acid decreased metabolic parameters evoked by MSG. After obesity induction, there was recorded significant growth of cholesterol, triglycerides, and LDL cholesterol blood levels and significant decline in HDL cholesterol blood levels. There was a significant reduction in triglycerides, LDL cholesterol and VLDL, in 2-[4-(benzyloxy) phenoxy] acetic acid - treated group. Our results represent the basis for development of new treatment of obesity and associated conditions.

Sex-based differences in phagocyte metabolic profile in rats with monosodium glutamate-induced obesity

The important component of obesity pathogenesis is inflammatory activation of innate immune cells within adipose tissue and in other body locations. Both the course of obesity and innate immune reactivity are characterized by sex-associated differences. The aim of the work was a comparative investigation of metabolic profiles of phagocytes from different locations in male and female rats with MSG-induced obesity. The administration of monosodium glutamate (MSG) caused obesity, with sex-associated differences, that was more severe in male rats. Obesity was associated with pro-inflammatory activation of CD14+ phagocytes from adipose tissue in female, but not in male rats, which was demonstrated by decreased phagocytosis activity along with increased ROS generation. Phagocytes from the peritoneal cavity and peripheral blood of obese female rats exhibited neutral metabolic profile, whereas those cells from obese male rats displayed a pro-inflammatory metabolic profile. Thus, the manifestation of obesity-induced inflammation was characterized by different patterns of metabolic profile of phagocytes in male and female rats. Identified immune cell characteristics expand our knowledge of obesity immunobiology and may help to develop more effective preventive and therapeutic interventions for obese patients of different sexes.

Efficacy of nanoceria for periodontal tissues alteration in glutamate-induced obese rats\u2014multidisciplinary considerations for personalized dentistry and prevention

BackgroundNowadays, we face the global epidemic of obesity, that is known to contribute to the development of many diseases, such as the oral cavity pathologies. Dental and oral pathologies are frequently caused by and overlapped with systemic multifactorial diseases such as obesity being its early indicators and risk factors.The aim was to study the influence of nanoceria on periodontal tissues alteration in glutamate (MSG)-induced obese rats.MethodsWe included 52 Wistar rats of both genders and divided into four groups: newborn rats in group 1 (control) received subcutaneously 8 μl/g saline. Group 2 received 3 to 4 mg/g MSG subcutaneously on the second, fourth, sixth, eighth, and tenth day of life; group 3—intragastric administration of nanocrystalline cerium dioxide at a dose of 1 mg/kg volume of 2.9 ml/kg against the background of glutamate-induced obesity; the fourth group of animals was treated with a solution of sodium citrate intragastric volume of 2.9 ml/kg (solvent of nanocrystalline cerium). We determined the total proteolytic activity, the total antitrypsin activity, the content-free fucose and glycosaminoglycanes (GAG), content of TBA-active of products, the content of oxidation-modified proteins (OMB), and catalase activity in the homogenate of soft periodontal tissues of rats.ResultsIntragastric injection of nanoceria prevents activation of proteolytic processes, reducing the catabolism of glycoproteins and proteoglycans of periodontal tissue in MSG-induced obese rats. Injection of nanoceria prevents activation of proteolytic processes, significantly decreases the total proteolytic activity, and inhibits the activation of free radical oxidation in periodontal tissues of rats compared with MSG-induced obesity model without corrections. Further, it significantly increases the total antitrypsin activity in periodontal tissues by 1.7 times, TBA-reagents by 1.7 times, and content of OMB by 1.4 times compared with glutamate-induced obese animals.ConclusionsMSG-induced obesity triggers periodontal tissue alterations in the rat model. Nanoceria contributes to the corrections of pathological changes in periodontal tissues in glutamate-induced obese rats via balancing protein-inhibitory capacity and reducing the depolymerization of fucosylated proteins and proteoglycans and antioxidative activity.

Probiotic strains of lactobacilli and bifidobacteria alter pro- and anti-inflammatory cytokines production in rats with monosodium glutamate-induced obesity.

The aim of this study was to investigate the effect of probiotic strains of Lactobacillus casei IMV B-7280, Bifidobacterium animalis VKL, B. animalis VKB on the pro- and anti-inflammatory cytokines production in Wistar male rats with monosodium glutamate (MSG)-induced obesity. It was established that neonatal administration of MSG to rats leads to increasing levels of the interleukin (IL)-1β and IL-12, and to decreasing ofthe IL-4, IL-10 and tumor growthfactor (TGF)-β levels in the bloodserum. After administration of the B. animalis VKL - B. animalis VKB - L. casei IMV B-7280 composition to obese rats the level of the IL-lP in blood serum wasn't differ from that in the obese rats, that didn't receive of the probiotic bacteria. But there was no statistically signifcant difference comparing with intact rats. The level of the IL-12B p4O in blood serum was decreased under influence of the B. animalis VKL - B. animalis VKB - L. casei IMV B-7280 composition (18.9%, p < 0.05) and B. animalis VKL (10.5%, p < 0.05) compared with obese rats, not receiving probiotic bacteria, but remained higher than in intact animals. After administration to obese rats ofthe B. animalis VKL - B. animalis VKB - L. casei IMV B-7280 composition the levels ofthe IL-4, IL- 10 and TGF-β increased in blood serum comparing with obese rats, not receiving probiotic bacteria. The level of the IL-10 also increased under influence of the B. animalis VKB, and IL-4 - under influence of the L. casei IMVB-7280. Our results suggest that these probiotic bacteria and probiotic composition are able to down-regulation the inflammation in rats with MSG-induced obesity but the strongest anti-inflammatory effects have probiotic composition. The ability of lactobacilli and bifdobacteria to alter the pro- and anti-inflammatory cytokines production, opens perspectives to create new treatments for obesity and metabolic syndrome based on probiotics.

Effects of polyphenol compounds melanin on NAFLD/NASH prevention.

One of the pathogenic mechanisms of the progression non-alcoholic liver disease (NAFLD) to nonalcoholic steatohepatitis (NASH) is the accumulation of reactive oxygen species (ROS). So, antioxidant therapy is necessary for successful treatment of the liver injury. We have paid attention to melanin produced by yeast Nadsoniella nigra strain X-1 as novel antioxidant and anti-inflammatory agents with low toxicity. In current study we aimed to investigate the preventive effect of melanin on the monosodium glutamate (MSG) induced NAFLD model in rats. The study was carried out on 45 Wistar rats that were divided into 3 groups: intact, MSG- and MSG+melanin groups (n=15 in each group). Newborn rats of MSG- and MSG+melanin groups were administered with MSG (4mg/g, 8μl/g, subcutaneously) at 2nd-10th days of life. Since the age of 1 month, rats of MSG-group were treated with water (0.25ml/100g), rats of MSG+melanin groups-with melanin (1mg/kg) dissolved in water (0.25ml/100g). had been performed intermittently (two-week courses alternated with two-week breaks) for 3 months. In 4-month rats anthropometrical parameters and visceral adipose tissue (VAT) mass were estimated. To assess morphological changes in liver we used NAS (NAFLD activity score). The content of pro-inflammatory cytokines (interleukin (IL)-1β, IL-12Bp40, interferon (INF)-γ) and anti-inflammatory cytokines (IL-4, IL-10, tumor growth factor (TGF)-β) were measured by ELISA. We found significantly lower total score (1.0±0.19 vs 3.33±0.36, p<0.001), degree of steatosis (0.73±0.18 vs 1.80±0.17, p<0.001) and manifestation of lobular inflammation (0.27±0.11 vs 1.20±0.17, p<0.001) due to NAFLD activity score in MSG+melanin group compared to MSG-obesity. NASH we confirmed only in 33.3% of rats with MSG-obesity that was significantly higher than after melanin (6.7%) administration (p=0.033). Melanin administration reduce amount of visceral fat on 44.5% (p<0.001) as compared to MSG-obesity group. Melanin reduced the content of IL-1β in rat serum and restored the level of anti-inflammatory cytokines (IL-10, TGF-β) to the control values. Thus, the administration of melanin can prevent development of NAFLD/NASH in rats with MSG-induced obesity and can be considered as possible novel therapeutic agents but further studies to confirm its action needed.

BDNF levels in adipose tissue and hypothalamus were reduced in mice with MSG-induced obesity

Objectives: To observe the expression of brain-derived neurotrophic factor (BDNF) in hypothalamic and adipose tissue in mice with monosodium glutamate (MSG)-induced obesity.Methods: The effects of hypothalamic lesions, specifically arcuate nucleus (ARC) lesions, induced by MSG injection were studied in male ICR mice at the neonatal stage. The following parameters were compared: body weight, body length, Lee's index, food intake, body temperature, fat weight, and levels of total cholesterol (CHOL), triglyceride (TG), low-density lipoprotein (LDL), high-density lipoprotein (HDL), and blood glucose (GLU). The BDNF expression levels in hypothalamic and adipose tissue were measured using western blotting.Results: Compared with the control group, the model group body had significantly higher weight, Lee's index, food intake, fat weight, CHOL, TG, LDL, HDL, and GLU levels. BDNF expression levels in hypothalamic and adipose tissue were markedly down-regulated in the model group.Discussion: BDNF may be closely associated with MSG-induced hypothalamic obesity.

Recombinant murine fibroblast growth factor 21 ameliorates obesity-related inflammation in monosodium glutamate-induced obesity rats.

The aim of this study is to investigate the role of FGF21 in obesity-related inflammation in livers of monosodium glutamate (MSG)-induced obesity rats. The MSG rats were injected with recombinant murine fibroblast growth factor 21(FGF21) or equal volumes of vehicle. Metabolic parameters including body weight, Lee's index, food intake, visceral fat and liver weight, intraperitoneal glucose tolerance, glucose, and lipid levels were dynamically measured at specific time points. Liver function and routine blood test were also analyzed. Further, systemic inflammatory cytokines such as glucose transporter 1 (GLUT-1), leptin, TNF-α, and IL-6 mRNAs were determined by real-time PCR. FGF21 independently decreased body weight and whole-body fat mass without reducing food intake in the MSG rats. FGF21 reduced blood glucose level, Lee's index, visceral fat, and liver weight, and improved glucose tolerance, lipid metabolic spectrum, and hepatic steatosis in the MSG-obesity rats. Liver function parameters including AST, ALT, ALP, TP, T.Bili, and D.Bili levels significantly reduced in the FGF21-treated obesity rats compared to the controls. Further, FGF21 ameliorated the total and differential white blood cell (WBC) count, serum C-reactive protein (CRP), IL-6, and TNF-α levels in adipose tissues of the obesity rats, suggesting inflammation amelioration in the in the obesity rats by FGF21. FGF21 improves multiple metabolic disorders and ameliorates obesity-related inflammation in the MSG-induced obesity rats.

PGC-1α may associated with the anti-obesity effect of taurine on rats induced by arcuate nucleus lesion

Objective: To observe the effect of taurine treatment in rats with monosodium glutamate (MSG)-induced obesity.Methods: Rats with MSG-induced obesity were administered taurine for five weeks. The Lee's index, food intake, blood pressure, body temperature, body mass index (BMI), fat weight, and triglyceride (TG), low density lipoprotein (LDL), and high density lipoprotein (HDL) levels were compared. The PGC-1α expression levels in white and brown adipose were measured using reverse transcription polymerase chain reaction and western blotting, and pathological changes in the arcuate nucleus and liver were examined.Results: Compared with the model group, BMI, TG, and LDL in the high and low taurine dose groups were significantly lower, while HDL was higher. Body temperature in the taurine treatment groups was higher, and blood pressure was lower. The weight of brown fat in the taurine treatment groups was significantly higher than in the model group, while the white fat weight was significantly lower. Compared with the control group, the PGC-1α levels in white and brown adipose were higher in the taurine treatment groups and more significantly up-regulated in brown adipose.Discussion: This study suggests that taurine prevents obesity in MSG-treated rats and may be closely associated with energy metabolism.

Short-term periodic consumption of multiprobiotic from childhood improves insulin sensitivity, prevents development of non-alcoholic fatty liver disease and adiposity in adult rats with glutamate-induced obesity.

BackgroundToday the impairment of metabolism and obesity are being extensively investigated due to the significant increase of the prevalence of these diseases. There is scientific evidence that probiotics are beneficial for human health. Thus, the aim of the study was to investigate the effect of multiprobiotic “Symbiter acidophilic concentrated” on obesity parameters in the rats under experimental obesity.MethodsThe study was carried out on 60 newborn Wistar rats, divided into 3 groups, 20 animals in each (females – n = 10, males – n = 10): intact rats, monosodium glutamate (MSG-) and MSG + probiotic group. Rats of intact group were administered with saline (8 μl/g, subcutaneously (s.c.)). Newborns rats of MSG-group and MSG + probiotic group were injected with a solution of MSG (4.0 mg/g) s.c. at 2nd – 10th postnatal days. The MSG + probiotic group was treated with 140 mg/kg (1.4 × 1010 CFU/kg) of multiprobiotic “Symbiter”. MSG-group was treated with 2.5 ml/kg of water (per os) respectively. Administration was started at the age of 4 weeks just after wean and continued for 3 month intermittently alternating two-week course of introduction with two-week course of break.ResultsNeonatal treatment with MSG caused a stunted growth in both MSG-groups, which manifested with significantly smaller naso-anal length compared to adult intact rats. There was no significant difference in weight between intact and MSG-groups on 120th day. The adiponectin level in the serum of rats with MSG-induced obesity decreased by 2.43 times (p = 0.001) in males and 1.75 (p = 0.020) in females. Concentration of leptin in adipose tissue were significantly higher by 45.9% (p = 0.019) and 61.2% (p = 0.009) respectively in males and females compared to intact rats. Our study has indicated that daily oral administration of multiprobiotic to neonatal MSG-treated rats by 2-week courses led to significant reduce of total body and VAT weight with subsequent improvement in insulin sensitivity and prevention of non-alcoholic fatty liver (NAFLD) development.ConclusionsThese results have shown that periodic treatment with multiprobiotic prevents the MSG-induced obesity and NAFLD development.

Pathophysiological aspects of the pancreas function in rats with monosodium glutamate-induced obesity

Our study demonstrates that neonatal treatment with monosodium glutamate (MSG) leads to the development of visceral obesity in adult rats. In rats’ pancreas of both sexes massive edema and inflammation were found, which are characteristic of acute pancreatitis. Marked intralobular and perivascular lipomatosis was also found. There was also marked leukocyte infiltration in rats with MSG-induced obesity. Morphometric analysis confirmed pathological changes in pancreatic tissue. The level of blood amylase, lipase and pancreatic amylase was increased by 92% (p&lt;0.001), 312% (p&lt;0.001) and 162% (p&lt;0.001). So, neonatal treatment with MSG leads to the development of pancreatitis in adulthood of rats. We concluded that the development of pancreatitis in rats with MSG-induced obesity is the result of increase of synthetic and secretory processes in pancreatic cells.

Effects of fibre-enriched diets on tissue lipid profiles of MSG obese rats

In order to investigate the influence of some fibre-enriched diets on tissue lipids in an animal model of obesity induced by the administration of monosodium glutamate (MSG), obese rats were fed diets containing 30% of Acha, Cassava, Maize and Plantain for five weeks and weight gain, feed intake and lee index were recorded. The lipid profiles of plasma, erythrocytes, kidney, heart and liver as well as hepatic 3-hydroxyl-3-methylglutaryl-CoA (HMG-CoA) reductase activity were measured. The diets significantly (p<0.05) reduced weight gain and lee index in the obese rats. Obesity-induced increase in plasma and erythrocytes lipid levels was significantly (p<0.05) reduced by these diets. MSG-induced obesity also resulted in a significant increase (p<0.05) in hepatic cholesterol level which was reduced by the diets. MSG-obesity was characterised by a significant (p<0.05) increase in cholesterol, triacylglycerol and phospholipids in kidney and this was reversed by the diets except Maize which did not reverse the increased cholesterol level. Only Acha reversed the obesity-induced increase in heart cholesterol and phospholipids. The increased activity of hepatic HMG-CoA reductase associated with obesity was also significantly (p<0.05) reduced by the diets. In conclusion, dyslipidemia associated with MSG-induced obesity could be attenuated by consumption of fibre-enriched diets.