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Query: UMLS:C0020505 (hyperphagia)
 6,116 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

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

In 1978, we designed a new elemental diet, ED-AC, which modified after Vivonex-HN with the co-operation of Ajinomoto Co., Japan and Morton-Norwich Co., U.S.A.. ED-AC is now being used widely in Japan for enteral hyper-alimentation, even in case of pediatric surgery. We have new prepared another elemental diet, this time for infants, ED-P (pediatric). The ratio of amino acids in both ED was determined according the proposal of Professor Goro Inoue, Department of Nutrition, Tokushima University. The application of ED, particularly for surgical patients, has been most effective. the use of this diet for enteral hyperalimentation should find a wide application in surgical and medical practice.
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PMID:New preparations of the elemental diet and the clinical application. 679 42

Monosodium glutamate (MSG) is a well-known flavor enhancer used in both Western and Eastern cuisines. Responsible for the 'umami' (delicious) taste, it is incorporated into a large number of solid and liquid savory foods. Experimental studies have established that the presence of added MSG in foods influences palatability, preference and selection. Sensory evaluation tests have shown that both traditional and novel foods get higher palatability ratings if MSG is added at an appropriate dose. In young adults, behavioral tests have shown that the acquisition of a liking for novel foods is facilitated by the addition of MSG to the recipe. In institutionalized elderly persons as well as hospitalized diabetic patients, the addition of MSG to target foods in a lunch meal induced an increased intake for those specific foods, with a subsequent decreased intake of foods presented later in the meal. In both populations, only prandial food selection was affected by MSG, but meal size (kJoules) remained the same. Experiencing the positive effects of MSG is thus possible without inducing hyperphagia. In conclusion, MSG can be used casually by the consumer in order to increase palatability, and it can also be used selectively by nutrition experts in order to orient food selection toward a healthy diet composition.
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PMID:Effects of monosodium glutamate on human food palatability. 992 37

To investigate the relationship between development of obesity and the small intestinal functions two experimental models of male Wistar rats were used in the present work: 1) early postnatally overfed rats, nursed from birth to weaning in small litters (SL, 4 pups/nest), and 2) neonatally monosodium glutamate treated rats (MSG 2 mg/g b.w. administered s.c. for 4 days after birth) submitted to the same early nutritional manipulation. After weaning, all animals had free access to a standard pellet diet and at 40 and 80 days of age their body weight, body fat content and food consumption as well as changes of the brush-border-bound duodenal and jejunal alkaline phosphatase (AP) activity were compared with parameters of the offsprings raised under normal feeding conditions (NL, 8 pups/nest). At 40 and 80 days of age the postnatally overfed pups from SL nests became heavier, displayed a significantly increased epididymal plus retroperitoneal fat pad weight (P<0.01) and significantly higher AP activity in both segments of the small intestine (P<0.01) in comparison with rats nursed in NL nests, although their mean daily food intake did not differ from that of non-obese rats during the postweaning periods examined. In contrast, the same treatment of MSG rats had only a small effect on late appearance of obesity, i.e. in early postnatally overfed and normally fed MSG rats a similar pattern of body weight, food intake, adiposity and AP activity was found after weaning. The effect of MSG-treatment was also accompanied by the appearance of normophagia, hypophagia and stunted growth on day 40 and day 80, respectively. Moreover, the size of fat depots and the increase of brush-border-bound AP activity in MSG rats belonging to the SL and NL groups was quantitatively similar to the values size of these parameters observed in SL obese rats subjected to early postnatal overnutrition. These results indicate that postnatal nutritional experience (overnutrition) may represent a predisposing factor in control rats from small litters for the development of obesity in later life. Permanently increased small intestinal AP activity observed after weaning in both models of obesity when hyperphagia is not present suggest that these functional changes and associated alterations in food digestion could be a component of regulatory mechanisms contributing to the maintenance of their elevated body fat weight.
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PMID:Obesity and changes of alkaline phosphatase activity in the small intestine of 40- and 80-day-old rats subjected to early postnatal overfeeding or monosodium glutamate. 1504 54

We evaluated the effects of splenectomy on glucose homeostasis in obese and non-obese rats. Obesity was induced by subcutaneous injections of monosodium glutamate (MSG; 4g/kg) in neonatal rats. Control (non-obese) animals received equimolar saline. Splenectomy (SPL) was performed at 21 or 60 days of life (SPL21 and SPL60) in MSG obese and non-obese groups. Glucose tolerance, insulin resistance (IR), adiposity, histology of white adipose tissue (WAT) depots and glucose-induced insulin secretion (GIIS) in isolated pancreatic islets were evaluated at 90 days of life. In non-obese, despite of hyperphagia, the spleen ablation reduced body weight gain and energy efficiency, without changes in GIIS or IR. Slight reduction in glucose tolerance and augmented adipocyte size in subcutaneous WAT was noted in non-obese SPL21 group. In MSG-SPL21 rats was observed augmented body weight gain and energy efficiency, without alter adipocyte size. In contrast, MSG-SPL60 rats had lower body weight gain, reduced energy efficiency and smaller adipocyte size in WAT visceral depot in relation to MSG non-operated. Spleen ablation reduced insulin plasma levels in the MSG-SPL21 and MSG-SPL60 groups. Moreover, splenectomy reduced GIIS and improved glucose tolerance in MSG-SPL21 group. In MSG-SPL60 rats were observed reduction in IR, without changes in GIIS, despite of elevated glucokinase expression in pancreatic islets. In conclusion, spleen ablation reduces body weight in non-obese rats and slightly modifies glucose homeostasis. In contrast, in MSG-induced obesity, absence of the spleen can ameliorate glucose tolerance and reduce insulin secretion, improving insulin sensitivity.
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PMID:Splenic participation in glycemic homeostasis in obese and non-obese male rats. 3286 51