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

1. Lactation is associated with an increase in the arterial blood concentration of L-alanine and L-glutamate, but a decrease in that of L-glutamine compared with the corresponding values for virgin rats. 2. Virgin rats fed a 'cafeteria diet' that induces hyperphagia have increased arterial concentrations of L-alanine, L-glutamate and L-glutamine. During lactation L-alanine and L-glutamate concentrations are even higher. 3. The removal of L-alanine is decreased in hepatocytes from lactating rats fed either a chow or cafeteria diet. 4. Measurements of arteriovenous differences across lactating mammary glands indicate that appreciable amounts of L-glutamine and L-alanine are extracted by the gland. 5. A high proportion of the L-alanine metabolized by isolated acini from fed lactating rats is converted into lipid. 6. Metabolism of L-alanine in acini from starved lactating rats is limited by the activity of pyruvate dehydrogenase. 7. It is concluded that L-alanine and certain other amino acids taken up by the gland in excess of the requirements for protein synthesis can be converted into lipid.
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PMID:Utilization of L-alanine and L-glutamine by lactating mammary gland of the rat. A role for L-alanine as a lipogenic precursor. 731 14

Glutamate-induced obesity of Wistar-rats is known to develop under normophagic and normoinsulinemic conditions, although hyperphagia and hyperinsulinemia are common to obese individuals. Rats of this obesity model show retarded growth, reduced mass of some organs, carcass and whole body as well as an extraordinary high fat content, whereas protein content is reduced. In this study, nitrogen (N) balance, urinary excretion of urea-N, ammonia-N, creatine-N and alpha-amino acid-N and plasma free fatty acid concentration of growing, glutamate-induced obese rats were determined. The main results were independent of frame of reference (mmol N/kg body mass; mmol N/kg0.75 metabolic body mass; N in % of nitrogen intake): Nitrogen intake, urinary excretion of alpha-amino acids and nitrogen excretion in faeces were equal between lean and obese rats. Nitrogen excretion in urine was elevated in obese rats, mainly resulting from increased amounts of urea and ammonia. Nitrogen balance was positive in both groups, but reduced in obese rats. These data point to normal digestion of food proteins, but an unusual high oxidative desamination rate of the absorbed amino acids in obese rats. Taking into account the various hormonal and nerval alterations in glutamate-induced obese rats, resulting e.g. in increased hepatic insulin concentration, the retained amino acid carbon should be channelled into hepatic fatty acid synthesis. Really, unfasted and overnight fasted obese rats showed elevated plasma free fatty acid concentrations. Channeling of amino acids into lipogenesis may explain the low muscle mass and striking fat accumulation--despite normophagia and peripheral normoinsulinemia--of growing, glutamate-induced obese Wistar-rats.
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PMID:Reduced, positive nitrogen balance and elevated plasma free fatty acid concentration in growing, glutamate-induced obese rats. 790 47

The neurological mechanisms associated with weight gain in animals have been extensively studied in mammals, but relatively little investigation has been carried out in birds. As in mammals, it has been shown that lesion of the ventromedial nucleus of the hypothalamus leads to hyperphagia and obesity in several species of birds. Likewise, bilateral lesions of the lateral hypothalamus result in aphagia and weight loss. Therefore, at the level of the hypothalamus, control of body weight appears to be controlled by similar neurological mechanisms in all homeothermic species via modulation of the sympathetic nervous system. Because of the role of the mammalian striatum in body weight regulation, body weight data from various manipulative studies in chickens were analyzed to see if these areas play a role in avian body weight regulation. In the first study, cycloheximide, glutamate, or saline was injected intracerebrally into 1-day-old chicks. In the second study, 3-day-old chicks received surgical ablation of the neocortex or kainic acid-induced lesions of the paleostriatum. Decreased body weight was noted in chicks that received injections of cycloheximide or glutamate, or kainic acid-induced lesions. The disruption in body weight in Experiment 1 might have been due to neurochemical pathology thought to occur in the paleostriatum. In the second experiment, lesions of the neostriatum or hyperstriatum, analogous to the neocortex in mammals, did not produce a difference in weight gain compared to controls. This preliminary work with kainic acid lesions in the chicken paleostriatum demonstrates a significant long-term decrease in body weight. As in mammals, the basal ganglia may have a role in body weight regulation.
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PMID:Avian telencephalon and body weight. 791 25

Lunch intake was followed in 31 matched pairs of hospitalized diabetic patients over four consecutive days. Pairs of patients were matched for type and duration of diabetes, gender, age and body mass index. Lunches were composed of appetizer, meat, vegetables, starch, cheese, bread and dessert; water, coffee, tea and lemon were available. One patient per pair was randomly ascribed to the experimental group and was served vegetable and starch dishes added with 0.6% monosodium glutamate (MSG). Lunch intake was measured by weighing amounts served and left-overs. Patients in the experimental group ingested more starch food than their matched controls, and less lemon juice and yogurt. However, the total energy load at lunch was not different between groups. This effect on meal time food selection replicates earlier observations made on elderly persons. It is suggested that manipulating palatability of various foods within a meal, and especially by using MSG, is an efficient way to affect food selection in the meal, without inducing hyperphagia.
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PMID:Monosodium glutamate affects mealtime food selection in diabetic patients. 880 Apr 82

We studied the feeding rhythms and feeding patterns of adult Long-Evans rats treated with monosodium glutamate (MSG) in their early post-natal period. This treatment is known to induce neuronal degeneration in the arcuate nucleus (ARC), a major hypothalamic site implicated in the regulation of feeding. Neonatal rats were treated intraperitoneally with MSG or saline (controls) alone on the first days of life. At age of 6 months, male control and male MSG rats were placed in our automatic feeding system, and the structure of feeding behavior and diurnal feeding rhythms were analysed. On a 24 hours basis, MSG rats ate less than control rats (-24%). This hypophagia resulted from a mild diurnal hyperphagia (+6%) and a pronounced nocturnal hypophagia (-34%). This hypophagia was the main consequence of a decrease of meal size in MSG rats (-37%) and was associated with an increase in meal duration (+52%). It was also associated with a total disappearance of the two feeding peaks that normally occur at light and dark onset in the rat (-90% 2 h after dark onset and -49% 2 h before light onset). These results indicate that neonatal treatment with MSG induces important changes in feeding patterns and feeding rhythms in the adulthood. These changes might be related to the disappearance of neurotransmitters located in the arcuate nucleus.
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PMID:Behavioral deficits in monosodium glutamate rats: specific changes in the structure of feeding behavior. 962 91

Genetic obesity is associated with increased neuropeptide Y (NPY) messenger RNA (mRNA) and decreased POMC mRNA in the hypothalamus of ob/ob and db/db mice, or impaired sensitivity to alphaMSH (derived from POMC) in the yellow agouti mouse. Acquired obesity can be produced by chemically lesioning the hypothalamus with either monosodium glutamate (MSG) in neonates or gold thioglucose (GTG) in adult mice. The present study examined whether elevated NPY mRNA and/or decreased POMC mRNA in the hypothalamus are associated with obesity due to hypothalamic lesions. GTG injection into adult mice produced a profound obese phenotype, including hyperphagia, increased body weight, and increased leptin mRNA and peptide, in association with reduced hypothalamic NPY mRNA and POMC mRNA. MSG treatment produced virtual elimination of NPY mRNA in the arcuate nucleus and a reduction of hypothalamic POMC mRNA, and led to elevated leptin. MSG pretreatment did not attenuate GTG-induced hyperphagia and obese phenotype. These results do not support a role for NPY-synthesizing neurons in the arcuate nucleus in mediating hypothalamic acquired obesity, but are consistent with the hypothesis that decreased activity of hypothalamic neurons synthesizing POMC play a role in mediating hypothalamic obesity.
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PMID:Hyperphagia and weight gain after gold-thioglucose: relation to hypothalamic neuropeptide Y and proopiomelanocortin. 979 56

The effects of the glutamate N-methyl-D-aspartate (NMDA) receptor antagonist (5R,10S)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclo-hepten-5, 10-imine (MK-801) on 2-deoxy-D-glucose-induced hyperphagia were investigated in rats. MK-801 significantly increased 2-deoxy-D-glucose-elicited eating. The facilitating effects of MK-801 on 2-deoxy-D-glucose-elicited feeding were not affected by coadministration of a nitric oxide (NO) precursor, L-arginine. Because NO synthase inhibitors inhibit 2-deoxy-D-glucose-induced hyperphagia and activation of the NMDA receptor leads to NO formation, our results suggest that blockade of the NMDA receptor increases 2-deoxy-D-glucose-induced hyperphagia, which is unrelated to inhibition of NO, and that NMDA receptors may play a role in satiety.
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PMID:Influence of the non-competitive NMDA receptor antagonist MK-801 on 2-deoxy-D-glucose-induced hyperphagia in rats. 1047 26

World-wide obesity has risen to alarming levels. The average weight of German conscripts now increases by almost 400 g/year. Similar data were obtained in Austria, Norway and the UK. The rising prevalence of obesity coincides with a rising popularity of protein-rich diets. On average, Germans consume meat at 100 kg/year. Children eat some threefold more protein than recommended; infants of 6 to 12 months receive daily up to 5 g/kg body weight of protein. We hypothesise that it is not the protein, but the amino acid glutamate that determines the propensity of obesity. Chronic hyperglutamataemia may intoxicate arcuate nucleus (AN) neurons, thereby disrupting the hypothalamic signalling cascade of leptin action, causing hyperphagia, obesity and hyperleptinaemia. Hyperleptinaemia also exerts sympathetic effects including blood pressure elevation that are mediated via mechanisms different from the hypothalamic system, and other symptoms of the 'metabolic syndrome'. This may happen even before birth when in small-for-gestational-age foetuses with impaired umbilical plasma flow, foetal hyperglutamataemia induces AN damage followed by later impairment of feeding regulation, hyperleptinaemia and symptoms that characterise the 'thrifty phenotype'. We suggest abandoning the flavouring agent monosodium glutamate and reconsidering the recommended daily allowances of protein and amino acids, particularly during pregnancy.
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PMID:Does high glutamate intake cause obesity? 1451 71

Branched-chain amino acids (BCAAs) are essential amino acids that play a major role in brain energy metabolism. This study was done to elucidate whether central injection of BCAAs influences feeding behavior in chicks. We found that the intracerebroventricular injection of leucine (200 microg) significantly stimulated food intake in neonatal chicks during 30 min postinjection. Additionally, the starting time of feeding and pecking rhythm after injection were significantly accelerated by leucine. In contrast, isoleucine and valine had no effect on ingestive response during experiment periods. Moreover, a metabolite of leucine (alpha-ketoisocaproic acid) at an equimolar concentration of leucine also did not increase food intake in chicks. These results suggest that leucine induces hyperphagia of neonatal chicks and it may be due to the synthesized glutamate by exogenous leucine.
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PMID:Central administration of leucine, but not isoleucine and valine, stimulates feeding behavior in neonatal chicks. 1469 64

Although nutritional support using nutrient enemas was recorded almost 3,500 years ago, the modern era of clinical dietetics commenced with the development of intravenous hyperalimentation by Dudrick et al. and the development of the chemically defined diet by Greenstein et al. Thereafter, clinical nutritional support became widely accepted as one of the basic tools of patient care, and knowledge of the metabolism of nutrients has been extended. In particular, the significance of micronutrients in systemic function, importance of gut function on the systemic metabolism and immune system, and involvement of amino acids and fat elements in the development and amelioration of specific disease status such as renal and hepatic failure have been recognized, and specific nutritional support has been created as a treatment strategy. In addition to knowledge of renal and hepatic failure or metabolic disorders, accumulated information on tumor metabolism and pathophysiology in cancer cachexia has also enabled cancer treatment using a nutritional approach. An enteral diet containing certain amino acids such as arginine or glutamate, omega-3 unsaturated fatty acids, and nucleic acids has been developed, and its clinical application under the new concept of "immunonutrition" has demonstrated reduction of the incidence of infection and shortening of hospital stay. Many questions on Immunonutrition remain to be answered such as its mechanism or optimal composition, although it is a promising field for future evolution. Currently, the assessment of nutritional status and gut function is required through lifelong education of medical doctors as well as the popularization of nutritional support teams. In the near future, tailor-made nutritional support will be required based on gene polymorphisms.
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PMID:[Advance and perspective of clinical nutrition]. 1502 60


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