RESUMO
The negative changes of obesity to the locomotor system are a major concern in the current scenario, where obesity and metabolic syndrome are recurrent in Western societies. A physical exercise is an important tool as a way to rehabilitate obesity, highlighting whole-body vibration, as it is an easy-access modality with few restrictions. In this sense, we sought to evaluate the effect of whole-body vibration on the extensor digitorum longus muscle on a monosodium glutamate-induced obesity model. The main findings of the present study are related to the ability of the treatment with vibration to reduce the obesogenic characteristics and slow down the dyslipidemic condition of the animals. Likewise, the vibration promoted by the vibrating platform was essential in the recovery of the muscle structure, as well as the recovery of the muscle's oxidative capacity, initially compromised by obesity.
Assuntos
Glutamato de Sódio , Vibração , Animais , Músculo Esquelético/metabolismo , Obesidade/induzido quimicamente , Obesidade/metabolismo , Ratos , Ratos Wistar , Glutamato de Sódio/metabolismo , Glutamato de Sódio/toxicidadeRESUMO
We evaluated the temporal profile of the flavor enhancers monosodium glutamate (MSG), disodium inosinate (IMP), disodium guanylate (GMP), and monoammonium glutamate (MAG). We also evaluated the ability of these flavor enhancers to enhance salty taste in solutions containing different reductions of sodium chloride. Four experiments were conducted using Central Composite Rotational Design (CCRD) with focus on two objectives: concentration of flavor enhancers (0% to 1%) and reduction of sodium chloride content (0% to 100%). A 0.75% saline solution of NaCl was used as a control. In each experiment, the treatments were evaluated by the intensity of salty and umami tastes using an intensity scale. Treatments, selected according to the results of CCRD, were analyzed using time-intensity (TI) and temporal dominance of sensations (TDS) analyses. Glutamates (MSG/MAG) showed greater capacity to enhance salty taste than treatments containing nucleotides (IMP/GMP). The intensity of umami taste, using all the examined flavor enhancers, showed a similar sensory profile. Temporal perception curves (TI and TDS) of salty and umami tastes also showed a similar temporal profile. The glutamic acid amino acids were better able to improve salty taste than nucleotides in any range of sodium chloride reduction. Flavor enhancers showed greater ability to increase salty taste in smaller reductions in sodium chloride content. PRACTICAL APPLICATION: This research expand the knowledge about the ability to enhance the salty taste of flavor enhancers in different reductions in sodium content, Beside that, will provide information about the time profile of flavor enhancers. This study provides scientific technical information on the ability to intensify the salty taste of flavor enhancers and can assist the industry to develop new low sodium products and encourage the scientific community to conduct future research on this subject.
Assuntos
Aromatizantes/metabolismo , Inosina Monofosfato/metabolismo , Cloreto de Sódio/metabolismo , Glutamato de Sódio/metabolismo , Aromatizantes/análise , Humanos , Inosina Monofosfato/análise , Cloreto de Sódio/análise , Glutamato de Sódio/análise , PaladarRESUMO
The metabolic syndrome is a group of metabolic alterations considered a worldwide public health problem. Organic selenium compounds have been reported to have many different pharmacological actions, such as anti-hypercholesterolemic and anti-hyperglycemic. The aim of this study was to evaluate the effect of p-chloro-diphenyl diselenide (p-ClPhSe)2, an organic selenium compound, in a model of obesity induced by monosodium glutamate (MSG) administration in rats. The rats were treated during the first ten postnatal days with MSG and received (p-ClPhSe)2 (10 mg/kg, intragastrically) from 45th to 51 th postnatal day. Glucose, lipid and lactate levels were determined in plasma of rats. Glycogen levels and activities of tyrosine aminotransferase, hexokinase, citrate synthase and glucose-6-phosphatase (G-6-Pase) were determined in livers of rats. Renal G-6-Pase activity was also determined. The purine content [Adenosine triphosphate (ATP), adenosine diphosphate (ADP) and adenosine monophosphate] and mitochondrial functionality in the liver were also investigated. p-(ClPhSe)2 did not alter the reduction in growth performance and in the body weight caused by MSG but reduced epididymal fat deposition of rats. p-(ClPhSe)2 restored glycemia, triglycerides, cholesterol and lactate levels as well as the glucose metabolism altered in rats treated with MSG. p-(ClPhSe)2 restored hepatic mitochondrial dysfunction and the decrease in citrate synthase activity and ATP and ADP levels caused by MSG in rats. In summary, (p-ClPhSe)2 had homeostatic effects on glucose metabolism and mitochondrial function alterations induced by MSG administration to rats.
Assuntos
Glucose/metabolismo , Homeostase/efeitos dos fármacos , Mitocôndrias/metabolismo , Obesidade/tratamento farmacológico , Compostos Organosselênicos/administração & dosagem , Glutamato de Sódio/efeitos adversos , Animais , Colesterol/metabolismo , Feminino , Humanos , Fígado/efeitos dos fármacos , Fígado/metabolismo , Masculino , Mitocôndrias/efeitos dos fármacos , Obesidade/etiologia , Obesidade/metabolismo , Ratos , Ratos Wistar , Glutamato de Sódio/metabolismo , Triglicerídeos/metabolismoRESUMO
Physical exercise represents an alternative way to prevent and/or ameliorate chronic metabolic diseases. Disruption of sympathetic nervous system (SNS) activity contributes to adiposity in obese subjects. Here, we verified the preventive effect of swimming training upon adiposity, adrenal catecholamine storage, and pancreatic islet function in obese monosodium glutamate (MSG)-treated rats. Male neonatal Wistar rats received MSG (4 mg/g body weight) during the first 5 days of life and, at weaning, half of the rats were submitted to swimming training, 30 min/day, 3 days a week, until 90 days of age (exercised rats: MSGex). Half of the rats were used as controls (sedentary group, MSGsd). Exercise training (ET) decreased insulinemia and fat deposition in MSGex, and increased adrenal catecholamine content, compared with MSGsd rats. Insulinemia during the ivGTT was lower in MSGex rats, despite a lack of difference in glycemia. Swimming training enhanced insulin release in islets challenged by 2.8-8.3 mmol/l glucose, whereas, at supraphysiological glucose concentrations (11.1-16.7 mmol/l), MSGex islets secreted less insulin than MSGsd. No differences in insulin secretion were observed following l-arginine (Arg) or K(+) stimuli. In contrast, islets from MSGex rats secreted more insulin when exposed to carbachol (100 µmol/l), forskolin (10 µmol/l), or IBMX (1 mmol/l) at 8.3 mmol/l glucose. Additionally, MSGex islets presented a better epinephrine inhibition upon insulin release. These results demonstrate that ET prevented the onset of obesity in MSG rats, probably by enhancing adrenal catecholamine levels. ET ameliorates islet responsiveness to several compounds, as well as insulin peripheral action.
Assuntos
Terapia por Exercício , Glucose/metabolismo , Ilhotas Pancreáticas/metabolismo , Obesidade/metabolismo , Obesidade/terapia , Glutamato de Sódio/efeitos adversos , Animais , Exercício Físico , Humanos , Insulina/metabolismo , Secreção de Insulina , Masculino , Obesidade/fisiopatologia , Ratos , Ratos Wistar , Glutamato de Sódio/metabolismo , Natação , DesmameRESUMO
AIMS: Glucagon-like peptide-1 (GLP-1) is an important modulator of insulin secretion by endocrine pancreas. In the present study, we investigated the effect of swim training on GLP-1 insulinotropic action in pancreatic islets from monosodium glutamate (MSG)-obese rats. METHODS: Obesity was induced by neonatal MSG administration. MSG-obese and control (CON) exercised rats swam for 30 min (3 times week(-1) ) for 10 weeks. Pancreatic islets were isolated by colagenase technique and incubated with low (5.6 mM) or high (16.7 mM) glucose concentrations in the presence or absence of GLP-1 (10 nM). In addition, GLP-1 gene expression in ileum was quantified in fasting and glucose conditions. RESULTS: Exercise reduced obesity and hyperinsulinemia in MSG-obese rats. Swim training also inhibited glucose-induced insulin secretion in islets from both groups. Islets from MSG-obese rats maintained GLP-1 insulinotropic response in low glucose concentration. In contrast, in the presence of high glucose concentration, GLP-1 insulinotropic action was absent in islets from MSG-obese rats. Islets from MSG-exercised rats showed reduced GLP-1 insulinotropic action in the presence of low glucose. However, in high glucose concentration swim training restored GLP-1 insulinotropic response in islets from MSG-obese rats. In all groups, glucose intake increased GLP-1 immunoreactivity and gene expression in ileum cells in relation to fasting conditions. Swim training reduced these parameters only in ileum cells from CON-exercised rats. Neither MSG treatment nor exercise affected GLP-1 expression in the ileum. CONCLUSIONS: Exercise avoids insulin hypersecretion restoring GLP-1's insulinotropic action in pancreatic islets from MSG-obese rats.
Assuntos
Peptídeo 1 Semelhante ao Glucagon/metabolismo , Obesidade/metabolismo , Condicionamento Físico Animal/fisiologia , Glutamato de Sódio/metabolismo , Natação/fisiologia , Animais , Animais Recém-Nascidos , Peptídeo 1 Semelhante ao Glucagon/farmacologia , Glucose/metabolismo , Insulina/metabolismo , Ilhotas Pancreáticas/efeitos dos fármacos , Ratos WistarRESUMO
The monosodium glutamate (MSG) neonatal administration in mice provides a model of obesity with impaired glucose tolerance (IGT) and insulin resistance. However, the inflammatory profile of cytokines produced from fat tissue and its relationship to the metabolic dysfunction induced by MSG have not yet been revealed. The aim of this study was to establish the inflammatory profile attributed to MSG by measuring the expression of adipokines in visceral fat and serum of 19-week-old mice as well as the peroxisome proliferator-activated receptors alpha and gamma (PPARα and γ). Some metabolic and biochemical parameters were also quantified. The MSG increased mRNA expression of interleukin-6 (IL-6), tumour necrosis factor-alpha (TNFα), resistin and leptin, but adiponectin did not exhibit any changes. In addition, impaired glucose tolerance, increased levels of insulin, resistin and leptin were observed in serum. Both PPARα and PPARγ were activated in MSG-induced obese mice, which might explain its inflammatory profile. However, liver transaminases were severely depressed, indicating that MSG may also induce liver injury, contributing to inflammation. The MSG neonatal neuro-intoxication in mice may thus provide a model of obesity and inflammation characterized by the dual activation of PPARα and PPARγ, which might offer new insights into the mechanism of inflammatory diabetes in obesity leading to steatohepatitis, as well as a suitable model to study the role of new therapeutic agents to prevent or reduce insulin resistance, the inflammatory state and liver steatosis.
Assuntos
Aditivos Alimentares/toxicidade , Inflamação/metabolismo , Obesidade/induzido quimicamente , Obesidade/metabolismo , Receptores Ativados por Proliferador de Peroxissomo/genética , Glutamato de Sódio/toxicidade , Adiponectina/sangue , Tecido Adiposo/fisiopatologia , Envelhecimento/patologia , Animais , Glicemia/metabolismo , Peso Corporal/efeitos dos fármacos , Diabetes Mellitus Tipo 2/metabolismo , Modelos Animais de Doenças , Fígado Gorduroso/complicações , Feminino , Aditivos Alimentares/metabolismo , Inflamação/sangue , Inflamação/complicações , Insulina/sangue , Resistência à Insulina/fisiologia , Gordura Intra-Abdominal/fisiopatologia , Masculino , Camundongos , Camundongos Obesos , Obesidade/complicações , Receptores Ativados por Proliferador de Peroxissomo/metabolismo , RNA Mensageiro/metabolismo , Glutamato de Sódio/metabolismoRESUMO
Different levels of insulin sensitivity have been described in several animal models of obesity as well as in humans. Monosodium glutamate (MSG)-obese mice were considered not to be insulin resistant from data obtained in oral glucose tolerance tests. To reevaluate insulin resistance by the intravenous glucose tolerance test (IVGTT) and by the clamp technique, newborn male Wistar rats (N = 20) were injected 5 times, every other day, with 4 g/kg MSG (N = 10) or saline (control; N = 10) during the first 10 days of age. At 3 months, the IVGTT was performed by injecting glucose (0.75 g/kg) through the jugular vein into freely moving rats. During euglycemic clamping plasma insulin levels were increased by infusing 3 mU.kg-1.min-1 of regular insulin until a steady-state plateau was achieved. The basal blood glucose concentration did not differ between the two experimental groups. After the glucose load, increased values of glycemia (P < 0.001) in MSG-obese rats occurred at minute 4 and from minute 16 to minute 32. These results indicate impaired glucose tolerance. Basal plasma insulin levels were 39.9 +/- 4 microU/ml in control and 66.4 +/- 5.3 microU/ml in MSG-obese rats. The mean post-glucose area increase of insulin was 111% higher in MSG-obese than in control rats. When insulinemia was clamped at 102 or 133 microU/ml in control and MSG rats, respectively, the corresponding glucose infusion rate necessary to maintain euglycemia was 17.3 +/- 0.8 mg.kg-1.min-1 for control rats while 2.1 +/- 0.3 mg.kg-1.min-1 was sufficient for MSG-obese rats. The 2-h integrated area for total glucose metabolized, in mg.min.dl-1, was 13.7 +/- 2.3 vs 3.3 +/- 0.5 for control and MSG rats, respectively. These data demonstrate that MSG-obese rats develop insulin resistance to peripheral glucose uptake.
Assuntos
Intolerância à Glucose/metabolismo , Glucose/metabolismo , Resistência à Insulina/fisiologia , Obesidade/complicações , Glutamato de Sódio/metabolismo , Animais , Glicemia/análise , Teste de Tolerância a Glucose , Masculino , Ratos , Ratos WistarRESUMO
Different levels of insulin sensitivity have been descrebed in several animal models of obesity as well as in humans. Monosodium glutamate (MSG)-obese mice were considered not be insulin resistant from data obtained in oral glucose tolerance tests. To reevaluate insulin resistance by the intravenous glucose tolerance test (IVGTT) and by the clamp technique, newborn male Wistar rats (N = 20) were injected 5 times, every other day, with 4 g/Kg MSG (N = 10) or saline (control; N = 10) during the first 10 days of age. At 3 months, the IVGTT was performed by injecting glucose (0.75 g/Kg) through the jugular vein into freely moving rats. During euglycemic clamping plasma insulin levels were increased by infusing 3 mU. Kg(-1). min (-1) of regular insulin until a steady-state plateau was achieved. The basal blood glucose concentration did not differ between the two experimental groups. After the glucose load, increased values of glycemia (p<0.001) in MSG-obese rats occurred at minute 4 and from minute 16 to minute 32. These results indicate impaired glucose tolerance. Basal plasm insulin levels were 39.9 + 4 muU/ml in control and 66.4 + 5.3 muU/ml in MSG-obese rats. The mean post-glucose area increase of insulin was 111 percent higher in MSG-obese than in control rats. When insulinemia was clamped, at 102 or 133 muU/ml in control and MSG rats, respectively, the corresponding glucose infusion rate necessary to maintain euglycemia was 17.3 + 0.8 mg. kg (-1). min(-1) for control rats while 2.1 + 0.3 mg. kg(-1). min(-1) was sufficient for MSG-obese rats. The 2-h integrated area for total glucose metabolized, in mg. min. dl(-1), was 13.7 + 2.3 vs 3.3 + 0.5 for control and MSG rats, respectively. These data demonstrate that MSG-obese rats develop insulin resistance to peripheral glucose uptake.