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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infusions of monosodium-L-glutamate into the rostral hypothalamus, believed to contain neurons mediating satiety, produced persistent hyperphagia and obesity, thus suggesting that a brain lesion had been produced. Similar infusions into the caudal hypothalamus, believed to contain unmyelinated axons of passage that mediate satiety, failed to alter food intake or body weight. Histological examination of the affected tissue confirmed the behavioral evidence that suggests that this technique spares axons but destroys cell bodies. Infusion of several other amino acids also damaged neurons while sparing axons of passage.
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PMID:Axon-sparing brain lesioning technique: the use of monosodium-L-glutamate and other amino acids. 91 Jan 44

Mice treated neonatally with monosodium-L-glutamate (MSG) are known to develop into obese adults without hyperphagia, which are characterized by the reduced levels in the resting metabolic rate (RMR) and the thermogenesis of brown adipose tissue (BAT) in the thermoneutral environment. The present study revealed that an acute cold-exposure (5 degrees C, 1 h) of these animals resulted in the increase in norepinephrine turnover and mitochondrial-5'-diphosphate (GDP) binding in the interscapular BAT as well as the guanosine RMR, suggesting a normal thermogenic responsiveness of BAT to cold.
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PMID:Effect of acute cold-exposure on norepinephrine turnover and thermogenesis in brown adipose tissue and metabolic rate in MSG-induced obese mice. 263 5

Mice treated with monosodium glutamate (MSG) in the neonatal period grow into obese, stunted adults without overeating. We have previously demonstrated normal control of brown adipose tissue (BAT) thermogenic function in the MSG-treated mouse and have concluded that thermoregulation at a lower than normal body temperature for most of the time is a major cause of its obesity. The objective of the present experiments was to find out whether adrenalectomy would prevent obesity in the MSG-treated mouse, as it does in hyperphagic obese rodents, and whether the thermoregulatory anomaly would be prevented by this procedure. MSG-treated mice that were adrenalectomized at 5 wk of age and studied at 10 wk of age did not become obese. Adrenalectomy increased body temperature of MSG-treated mice to normal (male mice) or almost normal (female mice). Adrenalectomy increased BAT mitochondrial guanosine 5'-diphosphate binding in MSG-treated mice, indicative of an increased thermogenic state, but had the same effect in control mice. We conclude that obesity in the MSG-treated mouse is secondary to the high level of corticosterone in its blood, which raises its metabolic efficiency, an effect of corticosterone also seen in normal lean mice, and causes it to thermoregulate at a low energy-conserving level. This latter effect is peculiar to the MSG-treated mouse and is not seen in corticosterone-treated normal mice.
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PMID:Adrenalectomy prevents obesity in glutamate-treated mice. 276 98

Inbred mice with the mutation diabetes C57BL/KsJ db+/db+ and the mutation obese C57BL/6J ob/ob displayed a total liver mitochondrial capacity to oxidize glutamate or succinate which was approximately eight times greater than the capacity of the C57BL/6J +/+ control mice. This increase in oxidation capacity was estimated by multiplying the observed twofold increase in each of the following components: total liver weight, the mitochondrial protein content per gram of liver, and glutamate or succinate respiration activity per milligram of liver mitochondrial protein. No significant difference in liver mitochondrial function and capacity for oxidation was observed between db+/db+ and ob/ob mutants, which indicated that these results may be primarily mediated by the genetic factors responsible for obesity and hyperphagia in these mutants, and not by the genetic traits associated with diabetes. These findings may provide a biochemical foundation in support of the thrifty gene hypothesis.
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PMID:Influence of genetic predisposition to diabetes and obesity on mitochondrial function. 287 79

Marked hyperphagia with an increase in the rate of body weight gain was noted in adult female rats 4 days after injections of 2 nmoles of kainic acid into the dorsal and ventral parts of hippocampus. The effect was still present 70 days later. At this time the increase in daily food intake and body weight gain amounted, respectively, to 39% and 93% over the control value. There was no change in water intake. The injection of kainic acid into only one part of the hippocampus--either dorsal or ventral--did not induce hyperphagia. Male rats with kainic acid lesion did not show changes in food intake or body weight gain as compared to vehicle-treated controls. In both sexes the degeneration of hippocampal perikarya induced by kainic acid was associated with a 50-60% decrease in glutamic acid decarboxylase activity and [3H]glutamate uptake, as well as with a small decrease in [3H]glutamate uptake in the hypothalamus, an area that receives glutamatergic fibers from the hippocampus. The results show that the hippocampus appears to play an important role in appetite motivation control by a mechanism which is sex-related.
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PMID:Role of the hippocampus in the sex-dependent regulation of eating behavior: studies with kainic acid. 378 11

Morphine stimulates food intake in mildly-deprived and nondeprived rats. Neonatal administration of monosodium glutamate (MSG) destroys the medial-basal hypothalamus and other circumventricular organs, including cells containing beta-endorphin that project to other hypothalamic nuclei proposed in the modulation of morphine hyperphagia. Food intake of MSG-treated and control rats were assessed following vehicle and morphine (1.0-5.0 mg/kg, sc) treatment in a mild (5h) food deprivation paradigm. Morphine hyperphagia was found to be absent in MSG-treated rats, although they responded normally to mild deprivation following vehicle treatment. These results add to the types of ingestive deficits observed in the MSG-treated rat, and suggest that the circumventricular system in general, and opioid medial-basal hypothalamic cells in particular may be implicated in morphine hyperphagia.
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PMID:Loss of morphine hyperphagia following neonatal monosodium glutamate treatment in rats. 395 19

In newborn mice subcutaneous injectionis of monosodium glutamate induced acute neuronal necrosis in several regions of developing brain including the hypothanamus. As adults, treated animals showed stunted skeletal development, marked obesity, and female sterility. Pathological changes were also found in several organs associated with endocrine function. Studies of food consumption failed to demonstrate hyperphagia to explain the obesity. It is postulated that the aduls syndrome represents a multifacted nueroendocrine disturbance arising from the disruption of developing nueral centers concered in the mediation of endocrine function.
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PMID:Brain lesions, obesity, and other disturbances in mice treated with monosodium glutamate. 577 21

Injection of 2-deoxy-D-glucose (2DG) elicits both analgesic and hyperphagic responses in rats. While pituitary dysfunction, decreased dopamine availability, or neonatal monosodium glutamate treatment decreases 2DG hyperphagia, they increase 2DG analgesia. In contrast, 2-DG analgesia alone is decreased by repeated 2-DG injections, while 2-DG hyperphagia alone is decreased following naloxone pretreatment. The present four experiments examined further mechanisms subserving these two induced responses. In the first experiment, rats were deprived of food for 6 h following 2-DG (600 mg/kg). While 2-DG hyperphagia persisted in the absence of glucoprivation, 2-DG analgesia failed to occur after this delay. In the second experiment, acute exposure to inescapable foot shock (4 mA, 0.5 s/5 s for 1 h) preceded administration of 2-DG (600 mg/kg). While 2-DG hyperphagia was eliminated by this procedure, 2-DG analgesia was significantly potentiated. In the third experiment, repeated morphine (10 mg/kg) injections over 14 days eliminated 2-DG analgesia on the fifteenth day, but failed to affect 2-DG hyperphagia. In the fourth experiment, lesions placed in either the lateral hypothalamus or zona incerta decreased 2-DG hyperphagia, but failed to affect 2-DG analgesia. These results are discussed in terms of common and dissociative mechanisms mediating both responses.
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PMID:Dissociation of analgesic and hyperphagic responses following 2-deoxy-D-glucose. 658 11

Neonatal administration of monosodium glutamate (MSG) produces in rats neurotoxic degeneration of the circumventricular system, including the medial-basal hypothalamus, depleting several neuropeptides and neurotransmitters in this area. In addition, a number of behavioral and neuroendocrine responses are impaired, including a significant decrease in the analgesic response to cold-water swims (CWS). The present study examined whether the alterations in the analgesic responses following CWS and 2-deoxy-D-glucose (2-DG) induced by neonatal MSG treatment were due either to direct alterations in a pain-inhibitory system, or alternatively, to alterations in a system that processes the stressful consequences or properties of a stimulus. To accomplish this, the analgesic, hypothermic, and locomotor responses following CWS and the analgesic, hyperphagic, and locomotor responses following 2-DG were assessed in rats treated neonatally (days 2, 4, 6, 8, and 10) with either MSG or a vehicle solution. MSG-treated rats displayed significant reductions in both their analgesic and hypothermic responses following CWS, suggesting that MSG treatment impairs an animal's ability to process sufficiently the stimulus properties of the swim as stressful. While MSG treatment potentiated 2-DG analgesia, it reduced 2-DG hyperphagia, suggesting that MSG treatment also impairs coping responses to glucoprivation. These data indicate the importance of the circumventricular system in the coding of stimuli as potential stressors and in the subsequent activation of requisite systems necessary to provide a sustained, coordinated, and synchronous coping response.
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PMID:Impairments in analgesic, hypothermic, and glucoprivic stress responses following neonatal monosodium glutamate. 673 8

Liver blood flow and exchange of oxygen, glucose, lactate, and amino acids were measured in pigs at the same time as the peripheral arteriovenous (A-V) difference of these substances was determined. Four groups of animals were studied; they were normal postabsorptive, septic fasted, and septic infused either with complete parenteral nutrition (4.25% mixed amino acid solution with 25% glucose) or an isocaloric solution of 1.8% leucine with glucose. Sepsis in the pig caused a rise in arterial concentration of all essential amino acids except tryptophan and a decrease of most of the others. The liver uptake of the sum of all amino acids rose from nonsignificant values to 26.03 mumol/min/kg at the same time as the peripheral A-V difference changed from +20.4 to -678.0 mumol/l. Hyperalimentation increased arterial amino acid concentration, whereas peripheral A-V difference decreased to -132.3 mumol/l. The total liver uptake of amino acids was 24.80 mumol/min/kg but with a higher proportion of essential amino acids than in the fasted septic state suggesting increased liver protein synthesis. When leucine and glucose were infused the peripheral A-V difference of the sum of all amino acids was only -45.6 mumol/l indicating an almost complete cessation of muscle proteolysis. The arterial plasma concentration of all amino acids except leucine, glutamine, and glutamate were markedly reduced. Although hepatic clearance rate of amino acids fell only slightly, due to the low plasma concentrations, the liver uptake decreased substantially to 7.37 mumol/min/kg suggesting a decreased liver protein synthesis which could be deleterious in the presence of sepsis.
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PMID:The effects of hyperalimentation and infused leucine on the amino acid metabolism in sepsis: an experimental study in vivo. 678 84


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