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

Three experiments were conducted to characterize the time course of amphetamine's effects on food consumption using procedures that would allow both decreases and increases in eating to be evident relative to control levels. In Experiment 1 we measured eating over 12 postinjection hr in rats. Orderly changes in within-day temporal patterns of eating over the 12 days of amphetamine administration suggest the role of conditioned adaptive processes. In Experiment 2, animals were not presented food until 2 hr after drug administration. Initial anorexia and subsequent hyperphagia were produced by repeated administration of amphetamine. Experiment 3 assessed both within-day and over-day changes in body weight and food consumption and showed that in addition to the drug's anorectic effect, amphetamine also reduces body weight via other mechanisms. In interpreting tolerance to anorectic drugs, it is necessary to evaluate such changes in body weight that indicate shifts in hunger that occur over days as well as shifts in within-day temporal patterns of eating that indicate the presence of conditioned adaptive changes. It is proposed that these two adaptive mechanisms account for pharmacodynamic tolerance.
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PMID:Amphetamine's effects on food consumption and body weight: the role of adaptive processes. 339 54

It has been easy to demonstrate, both in humans and animals, that the stresses which disturbed either the physiological homeostasis, the behavioural homeostasis or both simultaneously, induced the modifications of the food intake; these disorders often found expression in the inappropriate eating or, less frequently, in temporary anorectic phases. The most relevant hypotheses localized, in the anterior and median hypothalamus (paraventricular nuclei, ventral median nuclei, lateral hypothalamic area), the neurobiological mechanisms which were involved in this stress/eating behaviour relationship. In the brain, both aminergic and peptidergic systems were concerned; the stress-induced hyperphagia required the functionality of the dopamine, dorsal noradrenergic bundle and endogenous opioids of the central nervous system. The dramatic stress-induced anorexia was based upon the reciprocal actions of serotonin, norepinephrine and CRF systems. Other peptides, which some of them belonged to the brain-gut peptide group, could interfere with these mechanisms. The neuropeptides being common in the stress and eating physiological systems, the regulatory mechanisms were most coherent; nevertheless, the precise nervous structures and neurochemical circuits that produced the stress-induced hyperphagia or stress-induced anorexia, remain unknown.
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PMID:[Stress and feeding behavior]. 342 63

A 30% body surface area, open-flame, full-thickness burn of adult rats induced a 4-day period of anorexia that was followed by hyperphagia beginning on postburn day 10. The hyperphagic burned rats also exhibited increased resting energy expenditure and no gain in body weight, suggesting hypermetabolism. Plasma levels of immunoreactive insulin and albumin were decreased in both groups of burned rats; immunoreactive pancreatic glucagon concentrations were elevated only in the anorectic burned rats. Plasma levels of epinephrine were elevated in the hyperphagic burned rats. In the brain, dopamine metabolism appeared to be increased in the corpus striatum, nucleus accumbens, and amygdala of anorectic burned rats; norepinephrine levels were elevated in the hypothalamus and nucleus accumbens of the hyperphagic-hypermetabolic rats. These data indicate that this animal model of major burn trauma exhibits anorexia, hyperphagia, catabolism, and hypermetabolism. Furthermore, elevated dopamine metabolism appears to be associated with the anorexia, while the hyperphagia-hypermetabolism may be mediated by norepinephrine.
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PMID:Burn-induced alterations in feeding, energy expenditure, and brain amine neurotransmitters in rats. 357 6

Ru 24969 and two other putative 5-HT1B agonists 1-(3-chlorophenyl)piperazine (mCPP) and 1-[3-(trifluoromethyl) phenyl]piperazine (TFMPP) and RU 24969 dose-dependently decreased food intake over 4 h (and in the case of RU 24969 also over 24 h) in free-feeding male Sprague-Dawley rats. Decreasing the doses of the agonists below the range eliciting anorexia did not cause hyperphagia. The anorexic effect of RU 24969 over 4 h was antagonised by metergoline, (-)pindolol and (+/-)cyanopindolol, but not by ketanserin, spiperone or haloperidol. Metergoline and (+/-)cyanopindolol also antagonised the anorexic effect of RU 24969 over 24 h. This data is consistent with an action mediated by 5-HT1B receptors. Locomotor activity induced by RU 24969 was markedly antagonised by haloperidol despite its lack of effect on the anorexic response. Persistence of the anorexic effect of RU 24969 after p-chlorophenylalanine (pCPA) pretreatment suggests that 5-HT1B agonists induce anorexia at a postsynaptic 5-HT receptor.
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PMID:5-HT1B agonists induce anorexia at a postsynaptic site. 366 36

Several pieces of evidence indicate that brain serotoninergic systems play an inhibitory role in feeding, being specifically involved in regulating satiety and food selection. The anorectic drug fenfluramine has been shown to exert its effects by activating serotoninergic mechanisms. Since fenfluramine influences both central and peripheral serotonin stores, it is difficult to establish the relative contributions of the central and peripheral serotoninergic mechanisms in the regulation of feeding behaviour. In the present paper evidence is presented that changes in feeding come about In the present paper evidence is presented that changes in feeding come about after interventions in either the brain or the periphery. This evidence includes the observation that serotonin itself given subcutaneously causes a dose-related anorexia in rats trained to eat four hours a day, an effect antagonized not only by metergoline but also by xilamidine, a serotonin antagonist that does not cross the blood-brain barrier. Since serotonin given systemically cannot reach the brain, its effect is ascribed to the activation of peripheral mechanisms. Furthermore, as is the case with fenfluramine, subcutaneous administration of serotonin is able to completely counteract the overeating induced by the glucoprivic agents insulin and 2-deoxy-D-glucose (2-DG). It is concluded that activation of peripheral serotoninergic mechanisms is sufficient not only to reduce eating in rats trained to eat four hours a day, but also to control the hyperphagias brought about by insulin or 2-DG.
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PMID:Peripheral and central mechanisms of action of serotoninergic anorectic drugs. 374 Aug 35

A study was made of the main signs of food motivation in 132 patients with stages I-III essential hypertension on the basis of analysis of a special questionnaire: the patients were interviewed in hospital and after discharge (a total of 40-46 days) to reveal the effect of raised arterial pressure on food behavioral reactions. Clinical signs of a hypertensive crisis were noted in 87 patients, in 45 patients raised arterial pressure was not accompanied by a crisis. In 82% of the cases hypertensive reactions produced a marked effect on the manifestations of food motivation. Anorectic reactions prevailed in the first 3-6 days in 98 of 109 patients (80.7%). These reactions were pronounced and prolonged in the patients with normal body mass. During the second week hyperphagic reactions prevailed in 68% of the cases, their frequency, expression and period were greater in the patients with concomitant obesity. The revealed time course of food behavioral reactions reflected the phase of food motivation in patients with arterial hypertension: hypertensive anorexia followed by post-hypertensive hyperphagia for 2-3 weeks.
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PMID:[Clinical evaluation of changes in alimentary motivation and arterial pressure in patients with essential hypertension]. 382 98

The first 95 patients admitted to an inpatient Eating Disorders Program and diagnosed as having bulimia (binge eating only), bulimarexia (binging and purging), and anorexia nervosa (food restriction only) were evaluated for depression, suicidality, and family history. Major depression was found in 80% of patients; 20% had made suicide attempts in their life; and 40% of those attempting suicide made potentially lethal attempts. Patients with anorexia and bulimarexia tended to be younger, single, and Protestant. Patients with bulimarexia had overeating, oversleeping, more preoccupation with suicide, and more depression in their mothers. Patients with anorexia had more relatives with anorexia and bulimarexia, and patients with bulimia had more relatives with obesity. These findings suggest that eating disorders are unique disorders and not variants of affective disorder or alcoholism.
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PMID:Depression and suicidality in eating disorders. 385 65

Over the past years significant progress has been made in the treatment of childhood cancers due to newer and more intensive chemotherapeutic regimes. However, with the increased intensity of chemotherapy, more treatment related complications are seen, requiring also more aggressive supportive care. The major complications of the cytotoxic treatment are bone marrow aplasia, immunosuppression, vomiting, anorexia and weight loss and supportive measures as adequate blood component supply, prophylaxis, recognition and effective treatment of infections as well as parenteral hyperalimentation are corner stones of modern cancer therapy. Blood sampling, application of blood products or intravenous drugs and continuous parenteral nutrition is easily performed using a central venous line. Our experience with the continuous venous access of central lines in patients receiving aggressive cytotoxic treatment did not show a higher incidence of infectious complications but had significant advantages in the supportive care.
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PMID:[Supportive measures in aggressive cytostatic therapy]. 393 5

We report about a 76 years old patient with Cronkhite-Canada syndrome. The diagnosis has been found with the following clinical symptoms: diarrhea, anorexia, alopecia, and onychotrophia. Laboratory values: severe hypoproteinemia (total serum protein 4.3 g/dl, albumin 2.4 g/dl); endoscopical and radiological findings: a generalized polyposis which involved the whole intestine except the oesophagus. As far as we saw in our literature-overview of 55 patients with Cronkhite-Canada syndrome, this patient had for the first time a carcinoma of the urinary bladder and a Bricker operation 17 years before the onset of his disease. Further we remarked a lack in the resorption of the enterally administered thyroidal hormones. The progress was fatal despite a parenteral hyperalimentation and a treatment with antibiotics and glucocorticoids.
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PMID:[New observations in a case of Cronkhite-Canada syndrome]. 396 97

A discrete, ascending fiber system that supplies the hypothalamus with most of its noradrenergic terminals was destroyed at midbrain level, both electrolytically and with local injections of 6-hydroxydopamine, a destructive agent specific for catecholaminergic neurons. The result was hyperphagia leading to obesity. Fluorescence histochemical analysis showed that loss of noradrenergic terminals in ventral bundle termination areas such as the hypothalamus was necessary for hyperphagia. Damage to dorsal bundle or dopaminergic projections was not. Prior treatment with desmethylimipramine to selectively block uptake of 6-hydroxydopamine into noradrenergic neurons prevented both hyperphagia and loss of norepinephrine fluorescence. The lesions that produced hyperphagia also reduced the potency of d-amphetamine as an appetite suppressant. It is concluded that this noradrenergic bundle normally mediates suppression of feeding, thereby influences body weight, and serves as a substrate for d-amphetamine-induced loss of appetite.
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PMID:Overeating and obesity from damage to a noradrenergic system in the brain. 451 36


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