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

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

1. Monosodium glutamate (MSG) was administered by various methods to mice and rats of various ages and the incidence of obesity was later measured. 2. Newborn mice were injected subcutaneously with 3 mg MSG/g body-weight at 1, 2, 3, 6, 7, and 8 d of age; 16% died before weaning. Of the survivors, 90% or more became markedly obese. Mean carcass lipid content was increased by about 120% in both sexes at 20-30 weeks old. In male mice, MSG treatment increased body-weight and epididymal fat pad weight, and greatly decreased adrenaline-stimulated lipolysis in isolated fat cells. Body-eright of females was not increased significantly. Food intake was not increased in either sex from weeks 13 to 15. Blood glucose level was not generally increased by MSG but some of the male mice had abnormally high values. 3. Obesity was not detected in the offspring of female mice that had received 100 g MSG/kg diet, either from 3 weeks before mating until weaning, or from the 14th day of pregnancy until weaning. 4. Intraperitoneal injection of 10 mg MSG/g body-weight (in two doses) at weaning increased carcass lipid content in female mice by 34% by 23 weeks of age, but female rats were not affected. 5. The addition of 20 g MSG/l to the drinking-water from weaning onwards did not increase carcass lipid content in female rats or mice. 6. The addition of 20 g MSG/kg diet from weaning onwards did not alter body-weight or carcass lipid content in male and female rats by 14 weeks of age. 7. The obesity induced in mice by MSG was not associated with hyperphagia, unlike genetic obesity and obesity induced by gold thioglucose (GTG). 8. All types of mouse studied, obese and lean, had essentially the same linear relationship between carcass water content and carcass lipid content. 9. Although MSG-obese mice could not readily be differentiated from normal mice by the increase in body-weight, which was only about 10% compared to 50-120% for genetic and GTG-induced obesity, the proposed schedule of injections in the newborn was almost 100% reliable in inducing a high extent of adiposity.
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PMID:The induction of obesity in rodents by means of monosodium glutamate. 110 64

Adipsin gene expression is severely diminished in certain forms of genetic and acquired rodent obesity. Common to many of these models of obesity is decreased sympathetic nervous system (SNS) activity. In addition, treatment of MSG obese mice with the sympathomimetic drug mixture ephedrine and caffeine restores adipsin deficiency to normal, while reversing obesity. Based on these observations, we hypothesized that adipsin gene expression might be regulated through changes in SNS activity with deficient adipsin gene expression in obesity being the result of impaired SNS activity. In the present study we used three models to assess the role of the SNS in regulating adipsin gene expression. First we exposed mice to the cold (4 degrees C), a potent activator of SNS activity. Second, we chemically sympathectomized mice with 60H-dopamine. Third, we treated mice with BRL 26830A, an atypical beta adrenoreceptor agonist. In contrast to our initial hypothesis, these studies demonstrate that alterations of SNS activity do not affect adipsin gene expression in normal mice. Neither increased SNS activity secondary to cold exposure nor decreased SNS activity resulting from sympathectomy alter serum adipsin concentration or adipsin mRNA levels in white (WAT) and brown adipose tissue (BAT). Surprisingly, treatment of lean mice with BRL 26830A decreases both adipsin serum concentrations and adipsin mRNA levels, suggesting a potential role for atypical beta adrenoreceptors in pathways that suppress adipsin expression in vivo. The significance of this observation with respect to adipocyte physiology is unclear at present. Future studies will be aimed at defining the molecular mechanisms by which BRL 26830A suppresses adipsin gene expression and the physiological significance of this effect.
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PMID:Alterations in sympathetic nervous system activity do not regulate adipsin gene expression in mice. 164 81

Monosodium glutamate (MSG) has been shown to alter several neuroendocrine functions in neonatally treated rats. To evaluate possible alterations in lipogenesis rate and lipoprotein lipase (LPL) activity, male and female rats were injected during the neonatal period with MSG or saline (controls). In male MSG rats, an increase in lipogenesis of liver and retroperitoneal adipose tissues was observed. Triton WR 1339 (an LPL inhibitor) administration decreased retroperitoneal lipogenesis in these animals. In female rats, MSG-treatment increased lipogenesis only in gonadal and retroperitoneal adipose tissues. No change was observed in hepatic lipogenesis and the Triton administration did not change retroperitoneal lipogenesis. LPL activity was increased in the gonadal and retroperitoneal adipose tissues in male and female MSG-treated rats. These data suggest that there is a specific sex-dependent response in the development of MSG-induced obesity.
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PMID:Effect of monosodium glutamate treatment during neonatal development on lipogenesis rate and lipoprotein lipase activity in adult rats. 177 58

In vivo deuterium magnetic resonance spectroscopy was used to measure fat utilization rates in diabetic and non-diabetic obese and non-obese mice. Monosodium glutamate-treated mice were used as a model for obesity, and diabetes was induced by administration of streptozotocin. Deuterium levels were enhanced by addition of D2O to drinking water (10% v/v) for a period of 14 days. The deuterium magnetic resonance signals of the body water and adipose tissue were then monitored to measure the rate of deuterium loss from the body. The rates of fat utilization for obese mice were significantly lower (75%, p less than 0.05) (halflife, t1/2 = 113 +/- 13 days) than the rates for non-obese mice (t1/2 = 30.0 +/- 9.0 days). The induction of diabetes caused a large (90%) but proportionally similar increase in fat utilization for both groups of mice (obese, t1/2 = 11.0 +/- 5.2; non-obese, t1/2 = 3.0 +/- 0.9). The results suggest that the induction of diabetes in obese mice does not affect the utilization of fat as a metabolic fuel. These preliminary studies indicate that deuterium magnetic resonance spectroscopy may be a useful technique for non-invasive determination of the rates of fat utilization in vivo.
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PMID:The use of in vivo 2H NMR spectroscopy to investigate the effects of obesity and diabetes mellitus upon lipid metabolism in mice. 253 3

Rats with bilateral electrolytic lesions in the general region of the ventromedial hypothalamic (VMH) nucleus develop hyperinsulinemia, excessive food intake and obesity. Monosodium glutamate (MSG) destroys neurons of the arcuate hypothalamic (AH) nucleus and produces hyperinsulinemic but hypophagic obesity. Bipiperidyl mustard (BPM) primarily destroys VMH neurons, but has produced only a slight obesity even when rats were maintained on high-fat diets. In the present study, rats treated with MSG (AH lesion) were hyperinsulinemic, moderately obese and hypophagic; BPM rats (primarily VMH lesion) were not different from controls when fed standard chow diets. However, MSG/BPM rats (AH + VMH lesion) were hyperinsulinemic, massively obese and hyperphagic. Thus, two components of the electrolytic lesion syndrome previously attributed to VMH damage (hyperinsulinemia and obesity) were reproduced simply by MSG treatment alone. The third component (hyperphagia) occurred only when both AH and VMH were lesioned, suggesting that neurons in both nuclei may perform a satiety function and may be able to substitute for one another in this respect. Since MSG treatment is required for all components of both obesity syndromes described here, this underscores the importance of MSG-sensitive neurons in mechanisms of obesity. The combined treatment approach also represents the first rat model of hyperinsulinemic, hyperphagic obesity that can be entirely produced by systemic administration of neurotoxins.
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PMID:Components of hypothalamic obesity: bipiperidyl-mustard lesions add hyperphagia to monosodium glutamate-induced hyperinsulinemia. 345 67

Monosodium glutamate and bipiperidyl mustard both produce mediobasal hypothalamic lesions and have been reported to alter the subsequent feeding behavior and/or insulin levels of treated animals. In our previous studies bipiperidyl mustard alone had no effects on insulin levels or feeding, but in combination with glutamate produced hyperphagic obesity. Administration of exogenous cholecystokinin octapeptide also has been shown to affect feeding behavior and plasma insulin. In order to determine if endogenous cholecystokinin played a role in the effects of glutamate or bipiperidyl mustard, concentrations of cholecystokinin in the pituitary glands of lesioned rats were measured. Bipiperidyl mustard alone increased cholecystokinin content while combined lesioning with glutamate prevented the increase. The potential role of cholecystokinin-containing elements of the hypothalamus and pituitary in modulation of feeding is discussed.
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PMID:Hypothalamic neurotoxins alter the content of immunoreactive cholecystokinin in pituitary. 356 52

After the publication of recent data on the higher cardiovascular mortality in the italian speaking region as compared to the rest of the country, the present study had for scope to search any differences in the nutritional habits of the population of the three main linguistic regions of Switzerland. The data where obtained from national enquiries (1977-1982) and gives informations about anthropometric parameters, quantity of food consumed and percentage of consumers for different food stuffs. The study reveals that swiss italian women are first in prevalence of obesity in Switzerland during the years 1979-1982. For what concerns the nutritional habits, the results are contradictory in the optic of cardiovascular prevention and are symptomatic of the double cultural influence: nordic with abundant meat and dairy products consumed and mediterranean with abundant cereal and olive oil consumed. Accent is put on the methodological limits of this study and on the necessity of epidemiological data for better guidance in health care politics.
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PMID:[Contribution to the study of food consumption in Ticino]. 359 Oct 4

Neonatal administration of monosodium glutamate (MSG) results in severe adenohypophyseal endocrine malfunction as a result of hypothalamic neurotoxic lesioning. The present study examined the effects of administration of MSG on the neurohypophyseal vasopressinergic (AVP) system and systolic blood pressure (SBP) in adulthood. Monosodium glutamate or hypertonic sodium chloride was administered to male and female rat pups on days 1, 3, 5, 7 and 9 after birth. MSG treatment produced several features characteristic of the MSG-toxicity syndrome, including obesity, anterior pituitary dysgenesis and hypogonadism. However, MSG did not alter neurohypophyseal AVP profiles: AVP content of the posterior pituitary and microdissected regions of the hypothalamus and brainstem were similar in MSG-treated and control rats. Furthermore, MSG treatment did not alter water intake, serum AVP concentration, or the ability to reduce urine output in response to water deprivation. Thus, despite insult to adenohypophyseal function by neonatal administration of MSG, the neurohypophyseal AVP system remained functionally intact. In contrast, neonatal treatment with MSG altered SBP in a sex dependent manner. Female MSG-treated rats, unlike male MSG-treated rats, exhibited consistent systolic hypotension when compared with the NaCl-treated or non-treated control rats at 6, 9 and 12 weeks of age. Despite this chronic hypotension in MSG-treated female rats, heart rate was not altered and serum AVP was not elevated. These observations suggest a resetting of the baroreflex, attributable to neonatal administration of MSG.
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PMID:Monosodium glutamate neurotoxicity: a sex-specific impairment of blood pressure but not vasopressin in developing rats. 375 44

An over-the-counter preparation containing ephedrine, caffeine, and theophylline was examined for thermogenic anti-obesity properties. Administration of the methylxanthines to MSG-induced obese mice for 6 wk had no effect on energy balance or body composition. In contrast, treatment with ephedrine alone caused losses of 14% in body weight and 42% in body fat, effects brought about mainly by a 10% increase in energy expenditure. These changes were accentuated when ephedrine was administered together with one or both methylxanthines: energy expenditure was increased by a further 10%, and led to a reduction of about 25% in body weight and 75% in body fat, while the total food intake and body protein were unaltered. These results indicate that dietary methylxanthines like caffeine and theophylline, although alone have little effect on energy balance, can nevertheless markedly potentiate the thermogenic anti-obesity effect of ephedrine and normalize the body composition of the obese to the lean levels.
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PMID:The thermogenic properties of ephedrine/methylxanthine mixtures: animal studies. 395 78


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