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

The disappearance of norepinephrine from the heart, interscapular brown adipose tissue (BAT), and pancreas has been examined in mice with monosodium glutamate (MSG)-induced obesity and in untreated controls. MSG-treated mice became obese in the absence of increased food intake and their core temperature was significantly lower compared to control mice. The rate of norepinephrine turnover following blockade of norepinephrine synthesis with alpha-methyl-para-tyrosine was significantly slower in heart and interscapular BAT of these mice than in untreated controls, but MSG had no effect on the pancreas. It is suggested that reduced norepinephrine turnover may be a major factor in the development of obesity after neonatal administration of MSG.
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PMID:Reduced norepinephrine turnover in mice with monosodium glutamate-induced obesity. 649 48

The present study reports various developmental and behavioral changes in the offspring of rat dams that received monosodium glutamate (MSG) in the drinking water all through the second and third trimesters of pregnancy. Three main effects were observed in the MSG exposed offspring: (1) juvenile obesity; (2) reduced general activity levels; (3) a specific type of learning disability in discrimination learning involving choice between simultaneously present positive and negative stimuli.
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PMID:Prenatal monosodium glutamate (MSG) treatment given through the mother's diet causes behavioral deficits in rat offspring. 654 Dec 12

The thermogenic response to noradrenaline administration was investigated at 25 degrees C in two models of obese mice (genetic ob/ob obesity of the ' QEC ' strain and monosodium-glutamate-induced obesity) and in their respective lean littermates. Subcutaneous injections of a low dose of noradrenaline (100 micrograms/kg body wt.) elevated metabolic rate by about 30% in both obese models but not in their respective lean counterparts. In contrast, the increase in metabolic rate after injections of a high dose of noradrenaline (600 micrograms/kg body wt.) was of a similar magnitude in both lean and obese animals: metabolic rate was increased by 70-80%. These results indicate that the overall whole body thermogenic capacity is unimpaired at room temperature in this ' QEC ' strain of ob/ob mice and in the hypothalamic damaged obese mice. Obesity in these models is therefore not associated with a reduced ability to respond to noradrenaline but could rather be due to a failure to release noradrenaline.
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PMID:Unimpaired thermogenic response to noradrenaline in genetic (ob/ob) and hypothalamic (MSG) obese mice. 673 59

Neuronal necrosis in the arcuate and ventromedial hypothalamus regions is easily induced in 1-day-old Chinese hamsters by the administration of monosodium glutamate (MSG). New-born Chinese hamsters injected with MSG showed no sign of obesity, even when grown up, but apparently developed a diabetic syndrome.
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PMID:Diabetic syndrome in the Chinese hamster induced with monosodium glutamate. 698 22

Feeding behavior, activity level, and thermoregulatory ability of mice made obese by neonatal administration of monosodium L-glutamate (MSG) were studied. The degree of obesity and other characteristics of the syndrome were found to depend on age, diet, and housing condition. Carcass fat determinations demonstrated the presence of obesity in all MSG animals; however, body weight was elevated over control levels only in adult mice caged in groups. Group-housed MSG animals also failed to increase food intake in response to food deprivation and were both hypoactive and hypothermic. INdividually caged MSG mice showed normal activity levels and body temperature, an attenuated response to food deprivation, and an enhanced response to a high-fat diet. Since MSG obesity may be the consequence of damage to the dopamine-rich arcuate nucleus of the hypothalamus, a second goal of the study was to measure central catecholamines and examined any changes in the MSG animal's behavioral responses to catecholaminergic drugs. Animals treated with MSG sustained some loss of hypothalamic dopamine, but no systematic relation between central catecholamines and behavioral aspects of the syndrome could be discerned.
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PMID:Behavioral and neurochemical effects of neonatal administration of monosodium L-glutamate in mice. 721 14

Using two different experimental feeding paradigms, patterns of diet selection were examined in rats given monosodium glutamate (MSG) as neonates. In both Experiment 1 and Experiment 2, rats received subcutaneous injections of either 4 mg/g MSG or distilled water on alternate days from Day 3 to Day 19 postnatally. As previously reported, MSG-treated rats were shorter and had a greater mean Lee Index of obesity than vehicle-injected control animals. When provided with a choice of separate sources of the three macronutrients, protein, fat and carbohydrate, MSG-treated rats comsumed significantly more carbohydrate and less protein than vehicle-injected controls. Similarly, MSG-treated animals given access to a carbohydrate (32% sucrose) solution in addition to a standard laboratory diet (ground Purina Laboratory Chow) took in a significantly greater proportion of their daily caloric intake from the carbohydrate solution than did controls. The pattern of diet selection in MSG-treated animals is contrasted with patterns of diet selection in animals with other forms of experimental obesity.
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PMID:Increased carbohydrate consumption induced by neonatal administration of monosodium glutamate to rats. 729 Feb 89

The regulation of body weight and composition involves input from genes and the environment, demonstrated, for example, by the variable susceptibility of inbred strains of mice to obesity when offered a high-fat diet. The identification of the gene responsible for obesity in the ob/ob mouse provides a new approach to defining links between diet and genetics in the regulation of body weight. The ob gene protein product, leptin, is an adipocyte-derived circulating protein. Administration of recombinant leptin reduces food intake and increases energy expenditure in ob/ob mice, suggesting that it signals to the brain the magnitude of fat stores. Information on the regulation of this protein is limited. In several rodent models of obesity including db/db, fa/fa, yellow (Ay/a) VMH-lesioned, and those induced by gold thioglucose, monosodium glutamate, and transgenic ablation of brown adipose tissue, leptin mRNA expression and the level of circulating leptin are increased, suggesting resistance to one or more of its actions. We have assessed the impact of increased dietary fat on circulating leptin levels in normal FVB mice and FVB mice with transgene-induced ablation of brown adipose tissue. We find that high-fat diet evokes a sustained increase in circulating leptin in both normal and transgenic mice, with leptin levels accurately reflecting the amount of body lipid across a broad range of body fat. However, despite increased leptin levels, animals fed a high-fat diet became obese without decreasing their caloric intake, suggesting that a high content of dietary fat changes the 'set point' for body weight, at least in part by limiting the action of leptin.
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PMID:Leptin levels reflect body lipid content in mice: evidence for diet-induced resistance to leptin action. 748 15

We have found previously that arotinolol, an alpha/beta-adrenergic blocker, increases blood flow in brown adipose tissue (BAT) in a similar extent as BRL 26830A, a beta 3-adrenoceptor agonist. We tested the hypothesis that arotinolol activates thermogenesis in BAT, leading to weight loss in monosodium-L-glutamate-induced (MSG-induced) obese mice and saline-treated controls. Six weeks of standard animal feed (CE-2) containing arotinolol hydrochloride (350 mg/kg CE-2), which reduced mean blood pressure in MSG-treated mice, significantly increased the mitochondrial protein content in BAT, and activated the specific and total binding of guanosine-5'-diphosphate (GDP) in BAT mitochondria, leading to a reduction of obesity in both MSG- and saline-treated mice vs. the control groups fed with CE-2 diet alone. However, six weeks of CE-2 diet containing propranolol hydrochloride (525 mg/kg CE-2) a non-selective beta-blocker, markedly reduced the specific and total binding of GDP in BAT mitochondria, leading to weight gain in both MSG- and saline-treated mice. These findings support the hypothesis, that arotinolol activates BAT thermogenesis, leading to weight loss.
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PMID:The alpha/beta-adrenergic receptor blocker arotinolol activates the thermogenesis of brown adipose tissue in monosodium-L-glutamate-induced obese mice. 752 Mar 14

The RNA content of the ventromedial hypothalamus (VMH), the lateral hypothalamic area (LHA), and the cortical neurons of male and female rats, neonatally treated with monosodium glutamate (MSG), were investigated. MSG (2 g/kg b.wt.) was injected subcutaneously to male and female rat pups daily for 5 days after birth. At 12 weeks of age a significant decrease of RNA content in the VMH cells and significantly increased body fat in neonatally MSG-treated animals were found. Correlation of these data showed a significant negative correlation between the body fat content and the RNA content in VMH neurons. The results a) confirm a closed relationship between the body fat content and the functional activity of VMH, b) indicate that obesity of neonatally MSG-treated animals should be due to decreased functional activity of the VMH cells.
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PMID:Body fat and RNA content of the VMH cells in rats neonatally treated with monosodium glutamate. 753 99

We studied the gene expression of the insulin-like growth factor (IGF)-I, IGF binding protein (IGFBP)-3 and growth hormone (GH) receptor (GHR)/GH binding protein (GHBP) in liver of rats treated neonatally with monosodium glutamate (MSG). The MSG-treated rats showed severe growth retardation and obesity compared to saline-injected controls. Serum IGF-I levels in MSG-treated rats were significantly lower than in the controls after 6 weeks of age (p < 0.01). IGF-I gene expression increased with age and was significantly lower in MSG-treated rats than in the controls (p < 0.01). IGFBP-3 gene expression was unaffected by age in both MSG-treated male rats and the controls, but was less in MSG-treated female rats than in their controls between 6 to 8 weeks of age. In our study of GHR/GHBP gene expression, MSG-treated rats of both sexes displayed a distinct 1.5 kbase band encoding GHBP RNA. We speculated that these changes reflect disruption of GH secretion in in vivo experimental models. Thus, MSG-treated rats are useful as in vivo models for study of the effect of GH disruption on developmental gene expression.
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PMID:Studies of gene expression in liver of insulin-like growth factor (IGF)-I, IGF binding protein-3 and growth hormone (GH) receptor/GH binding protein in rats treated neonatally with monosodium glutamate. 753 19


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