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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The administration of monosodium-L-glutamate (MSG) during the neonatal period is known to result in central nervous system lesions in the arcuate nucleus of the hypothalamus and the retina. Rodents so treated exhibit behavioral deficts and endocrinopathies including obesity, hypogonadism, hypothyroidism, pituitary atrophy, tail automutilation and diminished locomotor activity. Assessment of endocrine status revealed normal serum levels of glucagon, thyroid-stimulating hormone and luteinizing hormone, and diminished levels of thyroid hormones and growth hormone in MSG-treated rats. Prolactin levels were elevated in the glutamate-treated male rats. Within the brain hypothalamic levels of thyrotropin-releasing hormone, luteinizing hormone-releasing hormone, and somatostatin were unchanged. Measurement of neurotransmitters and neurotransmitter-related enzymes in individual hypothalamic nuclei derived from MSG-treated rats revealed normal levels of norepinephrine, serotonin and glutamic acid decarboxylase, but reduced levels of choline acetyltransferase and dopamine in the arcuate nucleus and median eminence. Histochemical methods for visualization of dopamine and acetylcholinesterase in the mediobasal hypothalamus confirmed these findings. The MSG-treated animals exhibited a normal diurnal rhythm of pineal serotonin N-acetyltransferase activity. These data indicate that the MSG-induced endocrine deficiency syndrome results at least partly from destruction of cholinergic and dopamingeric tuberoinfundibular systems in the hypothalamus.
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PMID:Models of neuroendocrine regulation: use of monosodium glutamate as an investigational tool. 3 35

According to most existing theories, the regulation of energy balance is achieved by control of energy intake. This study was undertaken to find out whether there was control of energy output as well. Food intake, energy balance and the feed efficiency of weanling female mice made obese with injections of gold-thioglucose and monosodium glutamate indicate that the obesity is primarly due to an increased energetic efficiency, and suggest that the hypothalamus plays a role in controlling energy output. In the case of treatment with MSG, a relative obesity was observed, i.e. an increase in body fat without any change in body weight. This indicates that the CNS centres for the regulation of body weight and body fat are probably not the same. It is suggested that MSG obesity will be a suitable model for comparative studies of body weight and the regulation of fat content. It is concluded that chemically induced obesity is due more to a lower metabolic rate than to an elevated food intake.
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PMID:Energy balances in obese mice. 38 1

Caloric regulation and the development of obesity were examined in rats which had received parenteral injections of monosodium glutamate (MSG) as neonates. Rats were injected with either 2 mg/g or 4 mg/g MSG on alternate days for the first 20 days of life. Lee Indices of obesity were calculated at 22, 70, and 130 days of age. Animals in the 4 mg/g group were significantly more obese than controls at all three ages. However, both food intake and body weight of this group were significantly lower than those of controls. In adulthood, the ability to regulate caloric intake was tested by allowing animals access to diets of varying caloric densities. While control animals maintained relatively constant caloric intakes across dietary conditions, MSG-treated animals demonstrated an inability to respond to caloric challenges. Treated animals decreased caloric intake on a diluted diet and consumed more calories than controls when presented with a calorically dense diet. This inability to regulate caloric intake is compared with regulatory deficits observed in animals sustaining lesions of the ventromedial hypothalamus. The value of an animal model of juvenile-onset obesity is also discussed.
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PMID:Juvenile-onset obesity and deficits in caloric regulation in MSG-treated rats. 49 87

1. The syndrome of obesity induced by neonatal injection of monosodium glutamate (MSG) has been further studied in mice. In confirmation of previous studies stunting and decreased pituitary and gonadal weights were observed. 2. After weaning food intake was consistently less in MSG-treated than control mice. Body lipid stores were significantly elevated in MSG-treated mice by 2 weeks of age and increased progressively up to 4 months. 3. Plasma glucose was comparable between MSG-treated and control mice in the fed state whereas after an overnight fast MSG-treated mice exhibited relative hypoglycaemia. 4. Obese MSG-treated mice did not exhibit resistance to exogenous insulin and disposed of an intravenous glucose load more rapidly than control mice. 5. Hyperinsulinaemia was present inconsistently in both fed and fasted mice and in response to administered glucose. 6. Neonatal administration of MSG provides a useful additional model for studying the role of the hypothalamus in obesity.
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PMID:Effects of monosodium glutamate-induced obesity in mice on carbohydrate metabolism in insulin secretion. 63 58

Oxygen consumption and locomotor activity were studied in mice developing obesity after neonatal administration of monosodium glutamate (MSG) and in untreated controls. MSG-treated mice became obese in the absence of increased food intake. Locomotor activity was significantly less in MSG-treated mice 2, 10, and 20 wk after weaning. Oxygen consumption expressed in terms of the Lee index was not significantly different at 2 wk after weaning although at 10 and 20 wk it was significantly lower in MSG-treated mice. Plasma thyroxine was not different between MSG-treated and control mice. It is suggested that diminished energy expenditure is the major factor in the etiology of obesity after neonatal administration of MSG.
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PMID:Measurement of oxygen consumption and locomotor activity in monosodium glutamate-induced obesity. 64 5

Various dosages of monosodium glutamate (M.S.G.) were injected to 5 day old male chicks. Body weights, food intake, rate of obesity, semen production, some endocrine criteria and brain pathology were studied til 235 days post injection. All M.S.G. treated birds showed brain damage in the rotundus nuclei, and in the area located dorsolaterally to the ventromedial hypothalamic nuclei (V.M.H.). In some of the M.S.G. treated birds, additional brain regions were damaged, i.e. V.M.H., mammillary nuclei, dorsomedial anterior nuclei, ovoid nuclei, subrotundus nuclei, archistriatum and lateral forebrain bundles. Some of the M.S.G. treated birds showed marked abdominal fat deposition or low spermatozoan motility. It was impossible to attribute these changes to the dosage of M.S.G. injected. No significant differences were found in these parameters between the treated birds and the saline injected ones. When the M.S.G. treated birds were categorized on the basis of brain damage in specific sites, the following was observed: 1) Birds with V.M.H. damage accumulated significant larger amounts of fat in the abdominal adipose tissue than the rest of the M.S.G. treated birds. 2) Those M.S.G. treated birds, showing brain damage in their mammillary nuclei, produced semen of a very low spermatozoan motility rate as compared to the rest of the M.S.G. treated birds and the controls.
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PMID:The relation between monosodium glutamate inducing brain damage, and body weight, food intake, semen production and endocrine criteria in the fowl. 80 66

Infusions of monosodium-L-glutamate into the rostral hypothalamus, believed to contain neurons mediating satiety, produced persistent hyperphagia and obesity, thus suggesting that a brain lesion had been produced. Similar infusions into the caudal hypothalamus, believed to contain unmyelinated axons of passage that mediate satiety, failed to alter food intake or body weight. Histological examination of the affected tissue confirmed the behavioral evidence that suggests that this technique spares axons but destroys cell bodies. Infusion of several other amino acids also damaged neurons while sparing axons of passage.
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PMID:Axon-sparing brain lesioning technique: the use of monosodium-L-glutamate and other amino acids. 91 Jan 44

Administration of monosodium glutamate (MSG) to KK mice during the neonatal period resulted in a syndrome of obesity, stunting and hypogonadism. In some animals the genetic predisposition to diabetes was unmasked with the development of marked hyperglycaemia and or hyperinsulinaemia. Food intake was not increased compared to controls. The elevated plasma glucose and insulin in fed MSG treated mice fell rapidly with food deprivation. Glucose disposal was comparable in MSG treated and control mice after IP glucose, but after oral glucose MSG treated mice showed impaired glucose tolerance. Insulin secretion was defective in MSG treated mice after IP but not after oral glucose.
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PMID:Effects of monosodium glutamate administration in the neonatal period on the diabetic syndrome in KK mice. 100 51

Differential temperature measurement between interscapular brown adipose tissue (BAT, Tbat), rectum (Trect) and a subcutaneous point in the back left of the vertebral column (Tsc) was useful for examination of BAT-thermogenesis in glutamate-induced obese Wistar-rats. Positive temperature gradients Tbat-Tsc pointed to a basal BAT-thermogenesis, whereas negative temperature gradients Tbat-Trect did not indicate that heat production in lean and obese rats. One may conclude from this, that inclusion of subcutaneous points outside the BAT improves sensitivity of differential temperature measurements for BAT-thermogenesis. Basal temperatures Tbat, Trect and Tsc were reduced in obese rats compared to lean rats, although thermoinsulation of obese rats is improved on account of their high fat content. This points to a diminished heat production in obese rats. Cold exposure at 4 degrees C elicited an increase of temperature gradients Tbat-Trect in lean as well as in obese rats, with positive values found only in lean rats. However, positive values Tbat-Tsc were calculated for both groups. Increases were noted only in lean rats. Injection of noradrenaline (0.5 mg/kg i.m.) was followed by positive temperature gradients Tbat-Trect and increased positive values for Tbat-Tsc, pointing to a remarkable activation of BAT-thermogenesis in lean and obese rats. These findings confirm, that glutamate-induced obese rats preserved the ability to activate BAT-thermogenesis. There were, however, hints of reduced heat production in BAT of obese rats, thus contributing to obesity despite normophagia.
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PMID:Examination of brown adipose tissue thermogenesis of glutamate-induced obese rats by differential temperature measurements. 129 79

While numerous studies have examined sympathetic nervous system activity in experimental obesity, adrenal medullary function in this condition has received less attention. The experiments described herein evaluated adrenal medullary secretion by measurement of urinary epinephrine (Epi) excretion in genetically obese (ob/ob) mice and monosodium glutamate (MSG)-treated rats. In both male and female ob/ob mice Epi excretion was reduced 42% (P less than 0.015) and 47% (P less than 0.025), respectively, despite higher rates of urine output and excretion for other amines in obese compared to lean animals. In a similar fashion, urinary Epi was also lower in MSG-treated adult rats than in untreated controls; this reduction was out of proportion to group differences in body weight or excretion of other catecholamines. Administration of D,L-fenfluramine to mice, or dietary protein supplementation in rats, increased Epi excretion to the same extent in obese and lean animals. These findings indicate that secretion of Epi by the adrenal medulla is diminished, but is normally responsive to stimulation in these two models of animals obesity, and are thus consistent with accumulating evidence of a functional impairment in adrenal medullary secretion in animal and human obesity.
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PMID:Diminished epinephrine excretion in genetically obese (ob/ob) mice and monosodium glutamate-treated rats. 138 44


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