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

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

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

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

The study was aimed at investigating the effect of monosodium glutamate administered during the perinatal period on the reproductive system of sexually mature male rats. Monosodium glutamate (at a dose of 4 mg/g of body weight) or hypertonic saline was administered subcutaneously to newborn rats at 2--nd, 4-th, 6-th, 8-th and 10-th day of life. At the age of four months the rats were killed and histological and morphometric examinations of testes, epididymis, seminal vesicles and ventral prostate were carried out. Blood serum levels of LH, FSH, testosterone and 17-beta-estradiol were determined by radioimmunoassay. The administration of monosodium glutamate caused inhibition of growth, obesity and decrease in weight of pituitary glands and testes. Blood serum levels of and FSH as well as the height of epithelial cells of accessory sexual glands remained unchanged, whereas testosterone level was lowered.
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PMID:[Effect of perinatal administration of monosodium glutamate (MSG) on the reproductive system of the male rat]. 805 18

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.
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PMID:Monosodium glutamate (MSG)-obese rats develop glucose intolerance and insulin resistance to peripheral glucose uptake. 928 37

In order to evaluate the role of visceral and subcutaneous fat tissue in insulin sensitivity and lipid metabolism, we measured the fasting levels of plasma free fatty acid (FFA) and insulin, glucose disappearance rate (Rd), and hepatic glucose production rate (HGP) after surgical removal of visceral (VF) or subcutaneous (SF) fat tissue in monosodium glutamate-obese (MSG-Ob) rats. Monosodium glutamate obesity was induced in rats by neonatal injection of MSG. Surgery to remove fat was done at 15 weeks of age. The experiments were done four weeks after the surgery. MSG-Ob rats showed increased levels of FFA, insulin, and HGP and decreased Rd compared to normal rats. In the VF group, the FFA level and HGP were decreased to normal values, Rd was partially normalized, but the level of insulin did not change significantly compared to MSG-Ob. In the SF group, FFA and Rd were partially normalized, but HGP was not suppressed significantly compared to MSG-Ob. These results suggest that visceral fat affects the insulin sensitivity of liver and FFA concentration more than subcutaneous fat; however, no significant difference was shown on whole body insulin sensitivity and fasting insulin concentration.
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PMID:Surgical removal of visceral fat decreases plasma free fatty acid and increases insulin sensitivity on liver and peripheral tissue in monosodium glutamate (MSG)-obese rats. 1057 50

Monosodium glutamate (MSG) treatment of neonatal mice results in a selective damage to the arcuate nucleus (ARC) and development of obesity with increased adiposity at sustained body weight in the adulthood. Feeding pattern of the MSG obese mice is unusual. Our previous results showed that after 24-h fasting, MSG mice consumed negligible amount of food in several hours and therefore, it was impossible to register the effect of peptides attenuating food intake such as cholecystokinin (CCK) or cocaine- and amphetamine-regulated transcript (CART) peptide. To overcome this problem, two findings were used: firstly, orexigenic effect of neuropeptide Y (NPY) was attenuated both by CCK or CART peptide in lean fed mice and secondly, orexigenic effect of NPY was preserved in fed rats with MSG obesity. In this study, short-term food intake in fed lean and MSG obese C57BL/6 male mice was measured after simultaneous central administration of orexigenic NPY with either CART peptide or peripherally administered CCK. Anorexigenic action of exogenous CART peptide was preserved in MSG obese mice. On the other hand, satiety effect of exogenous CCK was completely lost in MSG obese mice. In conclusion, effective leptin signaling in ARC is necessary for satiety effect of CCK.
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PMID:Anorexigenic effect of cholecystokinin is lost but that of CART (Cocaine and Amphetamine Regulated Transcript) peptide is preserved in monosodium glutamate obese mice. 1909 18


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