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

The anorectic potency of naloxone and fenfluramine was evaluated in mice treated neonatally with 4 mg/g of MSG. Naloxone produced a specific and pronounced suppression of food intake in MSG-treated mice, whereas fenfluramine was equipotent in suppressing food intake for both MSG-treated and control mice. Naloxone at doses of 5, 10 and 20 mg/kg was significantly more potent in suppressing food intake in MSG-treated mice when compared to controls. Water intake, however was suppressed to a greater extent in control mice than MSG-treated mice following administration of either naloxone or fenfluramine. These results implicate endogenous opiate systems in the obesity and alterations in food intake regulation exhibited by MSG-treated mice.
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PMID:Naloxone-induced suppression of food intake is potentiated by neonatal administration of monosodium glutamate to mice. 666 10

The sequelae of neuroendocrine, somatic, and behavioral deficits following neonatal MSG treatment have been well-documented, including obesity and decreased locomotor activity. Recently, it was reported that increased body weight and decreased locomotor activity occurred only in group-housed animals. The studies reported here were designed to systematically explore the effects of housing conditions on MSG-treated mice. All aspects of the MSG syndrome were obtained, regardless of the housing condition. We conclude that housing variables play no role in the production of the MSG syndrome in mice. While all MSG-treatment mice had reduced brain weights (cerebrum) regardless of housing condition, MSG-treated mice raised individually had significantly lighter brains than MSG-treated mice raised in groups.
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PMID:The Monosodium L-glutamate (MSG) syndrome in mice develops independently of housing condition. 717 7

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

Non-insulin-dependent diabetes mellitus develops in obesity. The insulin resistance of this disease may be mediated by tumor necrosis factor-alpha (TNF-alpha). In particular, the TNF-alpha derived from adipose tissues might be involved in the induction of peripheral insulin resistance in rodent models of obesity. In general, monocytes/macrophages have been considered as the major source of TNF-alpha. This study was designed to examine the potential production of TNF-alpha from monocyte/macrophages in obese mice. In obese (ob/ob) and obese diabetic (db/db) mice, both of which are known to have severe insulin resistance, unstimulated serum bioactivity of TNF-alpha was significantly higher than that in lean control mice. Spontaneous TNF-alpha mRNA expression in splenic macrophages was also enhanced in obese mice, but not in monosodium-L-glutamate (MST)-induced obese mice which have no insulin resistance. In addition, both ob/ob and db/db mice produce more TNF-alpha than lean mice upon in vivo lipopolysaccharide (LPS) stimulation. The LPS-induced increase in serum TNF-alpha activity was not observed in MSG-induced obese mice. Taken together, it is postulated that TNF-alpha produced by monocytes/macrophages may also play an important role in the genesis of insulin resistance in obesity. Further study is needed to reveal the mechanism of enhanced TNF-alpha production in obese states and its possible etiologic relevance to obesity.
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PMID:Augmented production of tumor necrosis factor-alpha in obese mice. 788 92

We determined the response of glucose transport to insulin in isolated adipocytes and the lipogenic activity of insulin in fragments of epididymal adipose tissue obtained from male MSG-obese rats. Basal glucose transport rates (pmol 3 min-1 10(5) cells-1) were 100% higher in MSG than in control cells (3-month old male Wistar rats) pre-incubated for 30 min (P < 0.01). Nevertheless, when expressed as fmol 3 min-1 microns 2 cell surface area-1, transport rates were similar for the two groups (31.2 +/- 2.6 for MSG and 26.5 +/- 3.2 for controls, N = 7). No differences were observed in maximally insulin-stimulated glucose transport rates between groups (72.6 +/- 10.6 for MSG and 101.0 +/- 12.0 for controls, N = 7). In contrast, for adipocytes pre-incubated for 2 h, the basal uptake rates were 3.7 times higher and the maximal response to insulin was 103% higher in cells from MSG rats compared to control cells. These alterations in MSG rat adipocytes were accompanied by changes in cell sensitivity to insulin (EC50, 0.13 +/- 0.02 ng/ml for MSG vs 0.46 +/- 0.10 ng/ml for controls, P < 0.01). The rates of incorporation of labelled substrates (3H2O and 14C-glucose) into total lipids showed that in vitro lipogenesis was also 79% (3H2O) and 250% (14C-glucose) higher in MSG adipose tissue fragments. The MSG animals were consistently hyperinsulinemic. These data suggest that the obesity of 3-month old MSG rats is a metabolic alteration characterized by an enhanced adipocyte capacity to transport glucose and to synthetize lipids resulting in increased insulin sensitivity.
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PMID:Neonatal monosodium glutamate treatment increases epididymal adipose tissue sensitivity to insulin in three-month old rats. 800 Mar 47

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

Neonatal administration of MSG leads to a syndrome of endocrine dysfunction characterised by reduced growth, obesity and hypogonadism. The aim of the present investigation was to gain information on the structure and function of the pituitary-thyroid axis in MSG-treated rats. Neonatal Wistar rats received an s.c. MSG (4 mg/g body weight) or hyperosmotic saline (controls) on days 2, 4, 6, 8 and 10 of life. Histological and morphometrical studies were carried out on the thyroids of rats during the 4th month of life. Plasma TSH, T3, and T4 were measured by RIA kits. MSG-treated rats showed stunted growth, obesity and decreased pituitary weight. MSG administration resulted in increases in thyroid weight, absolute volumes of epithelium, colloid and stroma, and blood T3 level while T4 level remained unchanged. In enlarged thyroid gland, percentage fractions occupied by epithelium, colloid and stroma were similar to those observed in control rats. The results obtained suggest that the rat hypothalamic centres involved in regulation of the pituitary-thyroid axis are slightly affected by neonatal MSG treatment.
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PMID:Effects of neonatal treatment with MSG (monosodium glutamate) on hypothalamo-pituitary-thyroid axis in adult male rats. 830 23

Obesity is characterized by increased adipose tissue mass and is often accompanied by a number of other disorders, such as diabetes, hypertension, and hyperlipidemia. To investigate the interrelationship between excessive adipose tissue mass and these associated disorders, we have attempted to reduce adiposity via targeted expression of an attenuated diphtheria toxin A chain to adipose tissue, using the 5' regulatory region of the adipocyte P2 (aP2) gene. Transgenic mice with high levels of toxin expression developed chylous ascites and died shortly after birth. Transgenic mice expressing lower levels of the transgene had normal adiposity and survived to adulthood; however, they showed a complete resistance to chemically induced obesity. Nevertheless, these animals developed hyperlipidemia equal to or greater than their nontransgenic obese littermates. Moreover, MSG-treated transgenic females were fertile, unlike their obese nontransgenic littermates. These data demonstrate the feasibility of gentle manipulation of adiposity and allow a functional dissection of obesity and its metabolic sequelae.
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PMID:Targeted expression of a toxin gene to adipose tissue: transgenic mice resistant to obesity. 833 Jul 37

Changes in food intake, serum adipsin, and obesity were evaluated in the MSG-treated mouse. In Experiment 1, mice treated with MSG had 50% lower serum adipsin and over 2-fold higher percentage of body fat than the lean controls. Both feeding caffeine and restricting intake normalized serum adipsin and caused weight loss, but did not normalize the percentage of body fat. No additional effect was gained by feeding isoproterenol or ephedrine in combination with caffeine. In Experiment 2, we separated the direct effect of caffeine from the associated depression in intake using a paired feeding design, and also determined the effects of selected adrenergic agents and somatotropin (S). Somatotropin increased weight gain and reduced the percentage of body fat in healthy and obese mice, and tended to lower serum adipsin. Caffeine clearly depressed intake, caused weight loss, and increased serum adipsin, but similar results were achieved by restricting intake. None of the adrenergic drugs tested changed serum adipsin. Ephedrine depressed food intake and caused weight loss, but reduced the percentage of body fat only at the highest dietary concentration (2000 mg per kg of diet). Phenylephrine reduced weight gain without a concomitant effect on the percentage of body fat, and isoproterenol did not influence weight gain or body fat.
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PMID:Regulation of adipsin and body composition in the monosodium glutamate (MSG)-treated mouse. 891 74

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


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