Investigating the Role of the Hypothalamus in Outcomes to Repetitive Mild Traumatic Brain Injury: Neonatal Monosodium Glutamate Does Not Exacerbate Deficits.

Repetitive mild traumatic brain injury (RmTBI) is a prevalent and costly head injury particularly among adolescents. These injuries may result in long-term consequences, especially during this critical period of development. Insomnia and sleeping difficulties are frequently reported following RmTBI and greatly impair recovery. We sought to develop an animal model of exacerbated deficits following RmTBI by disrupting the hypothalamic circadian system. To accomplish this, we conducted RmTBI on adolescent rats that had received neonatal injections of monosodium glutamate (MSG), a known hypothalamic neurotoxin. We then examined behavioral, circadian, and epigenetic changes. MSG treated rats showed lower anxiety-like behaviors and displayed poor short-term working memory. We also showed changes in the morphology of the circadian clock in the suprachiasmatic nucleus (SCN) vasoactive intestinal polypeptide (VIP) immunostaining. VIP optical density in the SCN increased with MSG but decreased with RmTBI. There were changes in the expression of the clock genes and upregulation of the orexin receptors in response to RmTBI. MSG treated rats had longer telomere lengths than controls. Finally, although both MSG and RmTBI alone produced attenuated circadian amplitudes of activity and body temperature, exacerbated deficits were not identified in animals that received MSG and RmTBI. In sum, both MSG and RmTBI can alter behavior, circadian rhythm amplitude, SCN morphology, and gene expression independently, but the effects do not appear to be additive. Specific damage in the hypothalamus and SCN should be considered when patients experience sleeping problems following RmTBI, as this may improve therapeutic strategies.

Protective Effect Of Vitamin C On Monosodium Glutamate Induced Changes In The Oviduct Of Rats.

BACKGROUND: This study was conducted to evaluate the effect of Vitamin C on Monosodium Glutamate induced histopathological changes in oviduct of adult female Sprague Dawley rats. The duration of study was 6 months. It was an analytical experimental randomized control trial. METHODS: In this experimental study, 45 female adult Sprague Dawley rats of 10-14 weeks were used and divided into 3 groups. Each group contains 15 rats. Control group (C) received standard laboratory diet. Experimental group A, was given Monosodium Glutamate (0.08 mg/kg body weight/ day) whereas experimental group B, was served on both MSG and Vitamin C (250 mg/kg body weight/day). All groups received diet for a period of 4 weeks. After 4 weeks all rats were sacrificed and oviducts were obtained. For the study of tissue under light microscopy, tissue processing was done by using Haematoxylin and Eosin stain and 5micrometer thick sections were taken from the ampullary part of oviduct. RESULTS: After administration of MSG, group A showed vacuolization of epithelial cells, infiltration of RBCs in lumen with substantial decrease in the diameter of oviduct in group A. Protective effects were seen in vitamin C supplemented group B, with decrease in epithelial vacuolization and RBCs infiltrate along with increase in diameter of oviduct. CONCLUSIONS: Vitamin C has protective effect on Monosodium Glutamate induced histological changes in oviduct of rats.

Probiotics Supplemented with Omega-3 Fatty Acids are More Effective for Hepatic Steatosis Reduction in an Animal Model of Obesity.

Today probiotics have been suggested as a treatment for the prevention of NAFLD. Omega-3 fatty acid supplementation may have beneficial effects in regulating hepatic lipid metabolism, adipose tissue function and inflammation. The present study was designed to determine whether probiotics plus omega-3 are superior to probiotics alone on the monosodium glutamate (MSG)-induced NAFLD model in rats. We included 60 rats divided into four groups, 15 animals in each. Rats of group I were intact. Newborn rats of groups II-IV were injected with MSG. The III (Symbiter) group received 2.5 ml/kg of multiprobiotic "Symbiter" containing concentrated biomass of 14 probiotic bacteria genera. The IV (Symbiter-Omega) groups received "Symbiter-Omega" combination of probiotic biomass supplemented with flax and wheat germ oil (250 mg of each, concentration of omega-3 fatty acids 1-5 %). In both interventional groups reduction in total NAS score was observed. Supplementation of alive probiotic mixture with omega-3 fatty acids lead to 20 % higher decrease in steatosis score (0.73 ± 0.11 vs 0.93 ± 0.22, p = 0.848) and reduction by 16.6 % of triglycerides content in liver as compared to probiotic alone. Our study demonstrated more pronounced reduction in hepatic steatosis and hepatic lipid accumulation after treatment with combination of alive probiotics and omega-3 as compared to probiotics alone.

Taurine supplementation regulates Iκ-Bα protein expression in adipose tissue and serum IL-4 and TNF-α concentrations in MSG obesity.

PURPOSE: Obesity is usually associated with low-grade inflammation, which impairs insulin action. The amino acid, taurine (TAU), regulates glucose homeostasis and lipid metabolism and presents anti-inflammatory actions. Here, we evaluated whether inflammatory markers are altered in the serum and retroperitoneal adipose tissue of monosodium glutamate (MSG) obese rats, supplemented or not with TAU. METHODS: Male Wistar rats received subcutaneous injections of MSG (4 mg/kg body weight/day, MSG group) or hypertonic saline (CTL) during the first 5 days of life. From 21 to 120 days of age, half of each of the MSG and CTL groups received 2.5 % TAU in their drinking water (CTAU and MTAU). RESULTS: At 120 days of age, MSG rats were obese and hyperinsulinemic. TAU supplementation reduced fat deposition without affecting insulinemia in MTAU rats. MSG rats presented increased pIκ-Bα/Iκ-Bα protein expression in the retroperitoneal adipose tissue. TAU supplementation decreased the ratio of pIκ-Bα/Iκ-Bα protein, possibly contributing to the increased Iκ-Bα content in MTAU adipose tissue. Furthermore, MSG obesity or supplementation did not alter TNF-α, IL-1ß or IL-6 content in adipose tissue. In contrast, MSG rats presented lower serum TNF-α, IL-4 and IL-10 concentrations, and these alterations were prevented by TAU treatment. CONCLUSION: MSG obesity in rats was not associated with alterations in pro-inflammatory markers in retroperitoneal fat stores; however, reductions in the serum concentrations of anti-inflammatory cytokines and of TNF-α were observed. TAU treatment decreased adiposity, and this effect was associated with the normalization of circulating TNF-α and IL-4 concentrations in MTAU rats.

Fenugreek Seed Extract Prevents Fat Deposition in Monosodium Glutamate (MSG)-Obese Rats.

AIM: To evaluate the preventive effects of an aqueous extract of Trigonella foenum-graecum seeds (AqE-TFG) on fat deposition and dyslipidemia in monosodium glutamate (MSG)-obese rats. METHODS: Neonatal male Wistar rats were injected with MSG (4 g/kg b. w., subcutaneously) from day 2 to 14 after birth, on alternate days. From day 43 to 70, MSG treated rats were administered orally with AqE-TFG (0.5 and 1.0 g/kg b. w.). The anthropometric and biochemical parameters were analyzed on day 71. RESULTS: Treatment with AqE-TFG produced significant (P < 0.05 or P < 0.01) reduction in body weight gain, Lee's index, white adipose tissue (WAT) weights, adiposity index, blood glucose, serum insulin, leptin, lipids (low density lipoprotein cholesterol and very low density lipoprotein cholesterol), cardiac risk indexes (atherogenic index and coronary risk index), and homeostatic model assessment index. AqE-TFG treatment restored the activities of liver and epididymal WAT lipogenic enzymes (fatty acid synthetase and glucose-6-phosphate dehydrogenase) towards normal levels. Histological studies of liver also supported the experimental findings. CONCLUSION: These findings demonstrated the preventive effect of AqE-TFG on fat deposition and dyslipidemia possibly by improvement in glucose and lipid metabolism, enhancement of insulin sensitivity and down regulation of lipogenic enzymes.

Influence of diet supplementation with green tea extract on drug-metabolizing enzymes in a mouse model of monosodium glutamate-induced obesity.

PURPOSE: Consumption of dietary supplements with green tea extract (GTE) is popular for weight management, but it may be accompanied by various side effects, including interactions with drugs. The aim of the present in vivo study was to evaluate the effect of defined GTE (Polyphenon 60) in three dosage schemes on insulin, leptin and drug-metabolizing enzymes in obese mice. METHODS: Experimental obesity was induced by repeated s.c. application of monosodium glutamate to newborn mice. Green tea extract was administered in three dosage schemes in chow diet. The plasmatic levels of insulin and leptin were assayed using enzyme-linked immunosorbent assay. Enzyme activities and mRNA expressions of drug-metabolizing enzymes (totally 13) were analyzed in liver and small intestine using spectrophotometric and HPLC assays and RT-PCR, respectively. RESULTS: GTE-treatment decreased insulin and leptin levels. Eleven enzymes were significantly affected by GTE-treatment. Long-term administration of 0.01% GTE caused increase in the activity and mRNA level of cytochrome P450 3A4 (CYP3A4) ortholog in the liver as well as in the small intestine. Interestingly, short-term overdose by GTE (0.1%) had more pronounced effects on enzyme activities and mRNA expressions than long-term overdose. CONCLUSIONS: GTE-mediated induction of CYP3A4 ortholog, the main drug-metabolizing enzyme, could result in decreased efficacy of simultaneously or subsequently administered drug in obese individuals.

The effects of black garlic ethanol extract on the spatial memory and estimated total number of pyramidal cells of the hippocampus of monosodium glutamate-exposed adolescent male Wistar rats.

Monosodium glutamate (MSG) is believed to exert deleterious effects on various organs, including the hippocampus, likely via the oxidative stress pathway. Garlic (Alium sativum L.), which is considered to possess potent antioxidant activity, has been used as traditional remedy for various ailments since ancient times. We have investigated the effects of black garlic, a fermented form of garlic, on spatial memory and estimated the total number of pyramidal cells of the hippocampus in adolescent male Wistar rats treated with MSG. Twenty-five rats were divided into five groups: C- group, which received normal saline; C+ group, which was exposed to 2 mg/g body weight (bw) of MSG; three treatment groups (T2.5, T5, T10), which were treated with black garlic extract (2.5, 5, 10 mg/200 g bw, respectively) and MSG. The spatial memory test was carried out using the Morris water maze (MWM) procedure, and the total number of pyramidal cells of the hippocampus was estimated using the physical disector design. The groups treated with black garlic extract were found to have a shorter path length than the C- and C+ groups in the escape acquisition phase of the MWM test. The estimated total number of pyramidal cells in the CA1 region of the hippocampus was higher in all treated groups than that of the C+ group. Based on these results, we conclude that combined administration of black garlic and MSG may alter the spatial memory functioning and total number of pyramidal neurons of the CA1 region of the hippocampus of rats.

Is there a relationship between dietary MSG and [corrected] obesity in animals or humans?

The sodium salt of glutamate (monosodium glutamate; MSG) imparts a savory/meaty taste to foods, and has been used as a flavoring agent for millennia. Past research on MSG/glutamate has evaluated its physiologic, metabolic and behavioral actions, and its safety. Ingested MSG has been found to be safe, and to produce no remarkable effects, except on taste. However, some recent epidemiologic and animal studies have associated MSG use with obesity and aberrations in fat metabolism. Reported effects are usually attributed to direct actions of ingested MSG in brain. As these observations conflict with past MSG research findings, a symposium was convened at the 13th International Congress on Amino Acids, Peptides and Proteins to discuss them. The principal conclusions were: (1) the proposed link between MSG intake and weight gain is likely explained by co-varying environmental factors (e.g., diet, physical activity) linked to the "nutrition transition" in developing Asian countries. (2) Controlled intervention studies adding MSG to the diet of animals and humans show no effect on body weight. (3) Hypotheses positing dietary MSG effects on body weight involve results from rodent MSG injection studies that link MSG to actions in brain not applicable to MSG ingestion studies. The fundamental reason is that glutamate is metabolically compartmentalized in the body, and generally does not passively cross biologic membranes. Hence, almost no ingested glutamate/MSG passes from gut into blood, and essentially none transits placenta from maternal to fetal circulation, or crosses the blood-brain barrier. Dietary MSG, therefore, does not gain access to brain. Overall, it appears that normal dietary MSG use is unlikely to influence energy intake, body weight or fat metabolism.

A dietary restriction influences the progression but not the initiation of MSG-Induced nonalcoholic steatohepatitis.

The metabolic syndrome is a major worldwide health care issue and a dominant risk factor for cardiovascular disease. The liver manifestations of this syndrome include nonalcoholic fatty liver disease (NAFLD) and its progressive variant nonalcoholic steatohepatitis (NASH). Although significant research has been performed, the basic pathogenesis of NAFLD/NASH remains controversial and effective treatments are still unavailable. We have previously reported on a murine model of NASH induced by the neonatal injection of monosodium glutamate (MSG), which includes the clinical manifestations of central obesity, diabetes, hyperlipidemia, and ultimately liver inflammation, fibrosis, and cancer. Although MSG is considered a safe food additive, its administration to pregnant rats increases the voracity and growth hormone levels in the offspring. To further understand the biology of this model, we have investigated the influence of the calorie intake on these clinical manifestations by feeding animals a restrictive diet. MSG-treated animals fed a restrictive diet continue to manifest obesity and early stage NASH but have improvements in serum lipid profiles. At 12 months of age, mice had manifestations of obesity, whether animals were fed a restricted or control diet, but animals fed a restrictive diet had a reduction in the progression of NASH. In conclusion, MSG appears to be a critical factor in the initiation of obesity, whereas calorie intake may modulate the progression of disease.

Protective effect of Trigonella foenum-graecum Linn. on monosodium glutamate-induced dyslipidemia and oxidative stress in rats.

OBJECTIVES: The present study was designed to evaluate the effect of aqueous extract of Trigonella foenum-graecum(AqE-TFG) seeds on monosodium glutamate (MSG)-induced dyslipidemia and oxidative stress in Wistar rats. MATERIALS AND METHODS: Neonatal Wistar rats were treated subcutaneously with MSG (4 g/kg b.w.) from day 2 to 14 after birth, on alternate days. After attaining six-weeks of age, MSG-treated rats were administered with AqE-TFG (0.5 and 1 g/kg b.w., orally) or orlistat (10 mg/kg b.w., orally) for 28 days, respectively. Serum chemistry and relevant enzymes in hepato-cardiac tissues were assessed on day 29. RESULTS: AqE-TFG produced significant reduction in serum total cholesterol (TC), triglycerides (TGs), lactate dehydrogenase (LDH), aspartate amino transferase (AST), alanine amino transferase (ALT), hepatic and cardiac lipid peroxides (MDA) levels and elevation in serum high density lipoprotein cholesterol (HDL-C), hepatic and cardiac antioxidant enzymes [glutathione (GSH), and superoxide dismutase (SOD) and catalase (CAT)] levels. CONCLUSION: Results were comparable with orlistat, a standard anti-obesity drug, and provide clear evidence that the AqE-TFG treatment offered significant protection against MSG-induced dyslipidemia and oxidative stress, and may play an important role in amelioration of the free radical generated consequences like dyslipidemia and atherosclerosis.

Supplementing monosodium glutamate to partial enteral nutrition slows gastric emptying in preterm pigs(1-3).

Emerging evidence suggests that free glutamate may play a functional role in modulating gastroduodenal motor function. We hypothesized that supplementing monosodium glutamate (MSG) to partial enteral nutrition stimulates gastric emptying in preterm pigs. Ten-day-old preterm, parenterally fed pigs received partial enteral nutrition (25%) as milk-based formula supplemented with MSG at 0, 1.7, 3.0, and 4.3 times the basal protein-bound glutamate intake (468 mg·kg(-1)·d(-1)) from d 4 to 8 of life (n = 5-8). Whole-body respiratory calorimetry and (13)C-octanoic acid breath tests were performed on d 4, 6, and 8. Body weight gain, stomach and intestinal weights, and arterial plasma glutamate and glutamine concentrations were not different among the MSG groups. Arterial plasma glutamate concentrations were significantly higher at birth than after 8 d of partial enteral nutrition. Also at d 8, the significant portal-arterial concentration difference in plasma glutamate was substantial (∼500 µmol/L) among all treatment groups, suggesting that there was substantial net intestinal glutamate absorption in preterm pigs. MSG supplementation dose-dependently increased gastric emptying time and decreased breath (13)CO2 enrichments, (13)CO2 production, percentage of (13)CO2 recovery/h, and cumulative percentage recovery of (13)C-octanoic acid. Circulating glucagon-like peptide-2 (GLP-2) concentration was significantly increased by MSG but was not associated with an increase in intestinal mucosal growth. In contrast to our hypothesis, our results suggest that adding MSG to partial enteral nutrition slows the gastric emptying rate, which may be associated with an inhibitory effect of increased circulating GLP-2.

Dietary supplementation with monosodium glutamate is safe and improves growth performance in postweaning pigs.

Dietary intake of glutamate by postweaning pigs is markedly reduced due to low feed consumption. This study was conducted to determine the safety and efficacy of dietary supplementation with monosodium glutamate (MSG) in postweaning pigs. Piglets were weaned at 21 days of age to a corn and soybean meal-based diet supplemented with 0, 0.5, 1, 2, and 4 % MSG (n = 25/group). MSG was added to the basal diet at the expense of cornstarch. At 42 days of age (21 days after weaning), blood samples (10 mL) were obtained from the jugular vein of 25 pigs/group at 1 and 4 h after feeding for hematological and clinical chemistry tests; thereafter, pigs (n = 6/group) were euthanized to obtain tissues for histopathological examinations. Feed intake was not affected by dietary supplementation with 0-2 % MSG and was 15 % lower in pigs supplemented with 4 % MSG compared with the 0 % MSG group. Compared with the control, dietary supplementation with 1, 2 and 4 % MSG dose-dependently increased plasma concentrations of glutamate, glutamine, and other amino acids (including lysine, methionine, phenylalanine and leucine), daily weight gain, and feed efficiency in postweaning pigs. At day 7 postweaning, dietary supplementation with 1-4 % MSG also increased jejunal villus height, DNA content, and antioxidative capacity. The MSG supplementation dose-dependently reduced the incidence of diarrhea during the first week after weaning. All variables in standard hematology and clinical chemistry tests, as well as gross and microscopic structures, did not differ among the five groups of pigs. These results indicate that dietary supplementation with up to 4 % MSG is safe and improves growth performance in postweaning pigs.

The effect of monosodium glutamate on the cerebellar cortex of male albino rats and the protective role of vitamin C (histological and immunohistochemical study).

Monosodium glutamate (MSG) is a natural constituent of many foods and was reported to have neurotoxic effects. The aim of this study was to investigate the possible toxic effect of MSG on histological and glial fibrillary acidic protein (GFAP) immunohistochemical features of cerebellar cortex of albino rats and to evaluate the possible protective role of vitamin C against this effect. Thirty rats were divided into 3 equal groups. Group I, control; Group II, treated with 3 g/kg/day of MSG and Group III, received 100 mg/kg/day of vitamin C simultaneously with MSG. After 14 days, cerebellar tissues were obtained and processed to prepare sections stained with H&E, toluidine blue. The GFAP was detected immunohistochemically. Histological examination of group II showed degenerative changes as pyknotic Purkinje and granule cells with areas of degeneration surrounded by inflammatory cells in granular layer. However, group III showed more preserved histological structure of cerebellar cortex. Statistical analysis of area percent of the GFAP immunoreaction among studied groups showed significant increase in group III when compared with group I and group II. However, a non significant increase was detected in group II when compared with group I. In conclusion, MSG has neurotoxic effect leading to degenerative changes in neurons and astrocytes in cerebellar cortex of albino rats and vitamin C supplementation could protect from these changes. Getting more attention to the constituents of food products is recommended and vitamin C could be advised to protect people from food oxidants additives.

A novel rodent model that mimics the metabolic sequelae of obese craniopharyngioma patients.

Patients with craniopharyngioma (CP), a tumor located in the pituitary and/or hypothalamus, are susceptible to developing obesity and many metabolic complications. The study aim was to create a rodent model that mimics the complex neuroanatomical and metabolic disturbances commonly seen in obese CP patients. We compared the metabolic phenotype of animals with three distinct types of hypothalamic lesions: 1) destruction of the arcuate nucleus (ARC) induced by monosodium glutamate (MSG), 2) electrolytic lesion of the adjacent ventromedial nucleus (VMN) alone, 3) both the VMN and dorsomedial nucleus (DMN), or a 4) combined medial hypothalamic lesion (CMHL) affecting the VMN, DMN, and the ARC. Only the CMHL model exhibited all key features observed in patients with hypothalamic obesity induced by CP. These features included excessive weight gain due to increased adiposity, increased food intake, and pronounced hyperinsulinemia and hyperleptinemia. Similar to characteristics of patients with CP, CMHL animals exhibited reduced plasma levels of alpha-melanocyte stimulating hormone and reduced ambulatory activity compared with weight-matched controls. Therefore, the CMHL model best mimics the complex metabolic abnormalities observed in obese CP patients compared with lesions to other hypothalamic areas and provides a foundation for future pharmacological approaches to treat obesity in children with hypothalamic damage.

Effect of trans-fat, fructose and monosodium glutamate feeding on feline weight gain, adiposity, insulin sensitivity, adipokine and lipid profile.

The incidence of obesity and type 2 diabetes mellitus (T2DM) is increasing, and new experimental models are required to investigate the diverse aspects of these polygenic diseases, which are intimately linked in terms of aetiology. Feline T2DM has been shown to closely resemble human T2DM in terms of its clinical, pathological and physiological features. Our aim was to develop a feline model of diet-induced weight gain, adiposity and metabolic deregulation, and to examine correlates of weight and body fat change, insulin homeostasis, lipid profile, adipokines and clinical chemistry, in order to study associations which may shed light on the mechanism of diet-induced metabolic dysregulation. We used a combination of partially hydrogenated vegetable shortening and high-fructose corn syrup to generate a high-fat-high-fructose diet. The effects of this diet were compared with an isoenergetic standard chow, either in the presence or absence of 1.125 % dietary monosodium glutamate (MSG). Dual-energy X-ray absorptiometry body imaging and a glucose tolerance test were performed. The present results indicate that dietary MSG increased weight gain and adiposity, and reduced insulin sensitivity (P < 0.05), whereas high-fat-high-fructose feeding resulted in elevated cortisol and markers of liver dysfunction (P < 0.01). The combination of all three dietary constituents resulted in lower insulin levels and elevated serum ß-hydroxybutyrate and cortisol (P < 0.05). This combination also resulted in a lower first-phase insulin release during glucose tolerance testing (P < 0.001). In conclusion, markers of insulin deregulation and metabolic dysfunction associated with adiposity and T2DM can be induced by dietary factors in a feline model.

[Influence of jiangzhuo mixture on glucose and lipid metabolism in MSG obese-induced rats].

OBJECTIVE: To study the effect of Jiangzhuo Mixture (JZM) on glucose and lipid metabolism, free fatty acid (FFA) and insulin sensitivity index of sodium glutamate (MSG) induced obese rats. METHODS: Sixty-four male MSG rats, 8-10 weeks old, were randomly divided into 4 groups equally, the low dose and high dose JZM group were treated respectively with 10 mL/(kg d) and 20 mL/(kg d) JZM, the rosiglitazone (RGZ) group with water solution of RGE 20 mg/(kg d), while the model group fed only with distilled water 10 mL/(kg d) for control, all by gastrogavage for 7 successive weeks. Levels of fasting blood glucose (FBG), triglyceride (TG), cholesterol (TC), and serum fasting insulin (Ins) were measured before and after treatment. Besides, the level of FFA and the proportion of fat weight to body weight (F/B) were measured and insulin sensitivity index (ISI) was calculated after treatment. RESULTS: After being treated for 7 weeks, the indexes including TC, FBG, Ins, F/B and FFA were all lower than those in the model group. Compared with before treatment, TC level lowered, FBG and Ins level raised in the two JZM groups and the RGZ group. Comparisons between the three treated group showed a significant lower level of Ins in the RGZ group. Level of ISI was significantly lowered in the 3 groups after treatment (P <0.05), but still higher in the RGZ group than that in the model control group (P <0.05). As for level of FFA, it was 314.81 +/- 110.25 micromol/L in the high dose JZM group and 305.56 +/- 92.33 micromol/L in the RGZ group, which were lower than that in the low dose JZM group (375.00 +/- 219.95 micromol/L, P <0.05). CONCLUSIONS: JZM could decrease the serum levels of TC, FBG, Ins and FFA in MSG rats, and decrease the fat content of organism in rats' growth process. The FFA decreasing action is dose-dependent. But its effect on ISI in MSG rats in the growth stage is insignificant. JZM can not reverse the forming processes of hyperglycemia, hyperinsulinemia, and insulin resistance in MSG rats.

Adrenalectomy abolishes the food-induced hypothalamic serotonin release in both normal and monosodium glutamate-obese rats.

Corticosteroids influence energy homeostasis through centrally-mediated stimulation of energy intake and inhibition of expenditure, while central serotonin (5-HT) has opposite effects. Both serotonergic dysfunction and high glucocorticoid levels may be relevant in obesity. The neurotoxin monosodium glutamate (MSG) induces a non-hyperphagic and hypometabolic obesity with hypercorticosteronemia. We investigated the influence of corticosterone levels on the serotonergic system of MSG-obese and control rats. Applying microdialysis, we found a similar feeding-induced stimulation of serotonin release in the lateral hypothalamus (LH) in sham-adrenalectomized control and MSG rats. The concomitant serum corticosterone variations were markedly distinct between them, in that an increase occurred in the control group, while the initially high levels of the MSG rats decreased with feeding. It is suggested that this lowering of corticosterone prevented a higher serotonergic activation, which would lead to a higher meal-induced thermogenesis and a better adequation of the caloric intake to a low metabolism. Adrenalectomy completely abolished the feeding-evoked serotonergic stimulation in both groups. This observation demonstrates that glucocorticoids are necessary for food intake to acutely stimulate 5-HT release and indicates that serotonergic activity in the LH is not likely to participate in the adrenalectomy-induced attenuation of the MSG-obesity.

Efeito da vagotomia troncular em ratos injetados na fase neonatal com glutamato monossódico: estudo biométrico / Effect of truncal vagotomy in rats neonatally injected with monosodium glutamate: biometry study

Obesidade hipotalâmica pode ocorrer em humanos e pode ser reproduzida, experimentalmente, por lesão do VMH em ratos. Esta obesidade pode ser revertida por vagotomia troncular (VT), devido à redução da ingestão alimentar e da insulinemia mediada pelo nervo vago. Experimentalmente, a injeção de MSG causa lesão em nível de ARC. O objetivo deste trabalho é avaliar os efeitos do MSG em ratos e se VT os altera. Estudou-se 52 ratos Wistar machos, divididos em dois grupos de 26 animais, um submetido à injeção de MSG na fase neonatal e outro à de solução salina. Aos 30 dias de vida, após nova divisão, obteve-se: grupo MSG, submetido à VT (VTMSG), e outro à laparotomia (LAPMSG); grupo SALINA, submetido à VT (VTSAL), e outro à laparotomia (LAPSAL). Obteve-se peso, CNA e índice de Lee. O consumo alimentar foi obtido dos 30 aos 90 dias de vida. Aos 90 dias, após eutanásia, mensurou-se peso, CNA, índice de Lee e gordura perigonadal. Análise estatística foi realizada pelo "t de Student". Constatou-se que o MSG provoca redução do CNA e aumento do índice de Lee aos 30 dias de vida, e provoca redução do peso e do CNA, aumento do índice de Lee e da gordura perigonadal aos 90 dias e aumento do consumo alimentar dos 30 aos 90 dias de vida. A VT provoca redução do peso, do índice de Lee e da gordura perigonadal, e tendência à redução do CNA no rato injetado com MSG. A VT provoca redução de consumo alimentar nos primeiros 30 dias de pós-operatório, mas com tendência a maior consumo nos 30 dias subseqüentes. Conclui-se que o MSG injetado na fase neonatal provoca aumento do consumo alimentar e da adiposidade e causa redução da estatura e do peso do animal dos 30 aos 90 dias de vida. E que a VT, realizada aos 30 dias de vida, provoca redução do consumo alimentar nos primeiros 30 dias de pós-operatório, da adiposidade e do peso.