Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous behavioural studies have shown that 5-hydroxytryptamine3 (5-HT3) receptor antagonists either block or have no effect on amphetamine-induced effects. The present experiments investigated whether or not the highly selective 5-HT3 receptor antagonist ondansetron would affect the anorectic effect of a small dose (1 mg/kg) of d-amphetamine. Nondeprived male rats were tested in two feeding paradigms: consumption of a palatable sweetened mash and ingestion of a 3% sucrose solution. Ondansetron (10-100 micrograms/kg) did not antagonize amphetamine-induced anorexia; instead, in both paradigms consumption was reduced still further when the 5-HT3 antagonist was given in conjunction with amphetamine. Ondansetron given alone had significant effects on consumption, but the direction of the effect differed according to the paradigm. Sweetened mash intake was significantly increased at 30 and 100 micrograms/kg, while sucrose ingestion was significantly reduced at 10 and 30 micrograms/kg ondansetron. It is suggested that ondansetron has two opposing effects on intake, one of which (hyperphagia) can be masked by d-amphetamine, leaving an anorectic effect that augments that of d-amphetamine.
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PMID:The selective 5-HT3 receptor antagonist, ondansetron, augments the anorectic effect of d-amphetamine in nondeprived rats. 833 20

Long-term administration of sulpiride induces hyperphagia and obesity in female rats. After sulpiride withdrawal, a significant hypophagia has been observed. The hyperphagia could be related to the blockade and the hypophagia to supersensitivity of dopamine D2 receptors, in particular those D2 receptors located in the perifornical hypothalamus. If this were the case, an enhancement of anorexia induced by amphetamine and dopamine should be observed after interruption of long-term sulpiride treatment. Two doses of systemic sulpiride (20 or 200 mg/kg) and one dose of intrahypothalamic sulpiride (15 micrograms) were tested. Amphetamine was administered by systemic or intrahypothalamic infusion. Dopamine was administered in the hypothalamus. After withdrawal of systemic administration of sulpiride (200 mg/kg), an enhancement of anorexia induced by systemic amphetamine was observed. However, the anorexia induced by intrahypothalamic injections of amphetamine or dopamine was not affected by the interruption of the sulpiride treatment. These results suggest that the hypophagia following chronic sulpiride treatment is not due to supersensitivity of D2 dopamine receptors in the lateral hypothalamus. Moreover, the change in the response to amphetamine might be related to supersensitivity of extrahypothalamic D2 receptors.
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PMID:Enhancement of amphetamine anorexia after chronic administration of sulpiride in rats. 851 71

Hospitalized women with anorexia nervosa and/or bulimia nervosa and dietarily restrained and unrestrained, clinically normal women were provided with a multi-item breakfast meal. Eating patterns and hunger and satiety ratings were assessed. Subjects were offered three foods which varied in fat and carbohydrate contents. Anorectic-restrictors differed most from the control subjects: they had a longer meal duration, a slower overall rate of eating, more frequent pauses during the meal, and more short bouts of eating. They also displayed abnormal ratings of hunger and satiety: they were generally less hungry, had less urge to eat, and were more full than controls of bulimics. Both anorectic and bulimic patients showed more variability in total energy intake than did the controls. Patients usually displayed one of two patterns - either severe restriction or overeating. Abnormal hunger and satiety patterns indicating confusion typified the responses of bulimics; additionally, they showed more urge to eat in the post-meal period than did the controls. A higher proportion of fat in the initial part of the breakfast was related to a larger meal size for the bulimics. It is suggested that these techniques may be useful in evaluating the outcome of treatment for eating disorder patients.
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PMID:Micro- and macroanalyses of patterns within a meal in anorexia and bulimia nervosa. 866 30

Infections of the gastrointestinal nematode, Nippostrongylus brasiliensis, in the laboratory rat result in a characteristic biphasic anorexia which is followed by hyperphagia once the worm burden has been cleared. Despite the importance of parasite-induced anorexia, relatively little is known of the underlying mechanisms. We have investigated the involvement of the central appetite drive in this anorexia by studying the gene expression of two neuropeptides with opposing actions on energy balance, NPY and CRF. Gene expression was assessed by in situ hybridization at 2, 8 and 16 days post-infection (p.i.) in infected rats, in uninfected controls, and in a group with food intake restricted to match that taken voluntarily by the parasitize animals. The sampling intervals corresponded to each of the two phases of maximum anorexia and the period of compensatory hyperphagia. Surprisingly, we found that increases in NPY gene expression in the hypothalamic arcuate nucleus (ARC) accompany anorexia in rats infected with N. brasiliensis; there was a significant relationship between degree of anorexia and induction of NPY mRNA after 8 days of infection. Furthermore, ARC NPY mRNA levels in parasitized animals were similar to those in pair-fed individuals with food intake restricted to match the infected rats. The number of larvae used to establish the infection affected both the degree of anorexia and the level of NPY mRNA at 8 days p.i. in a dose-dependent manner. NPY gene expression remained elevated in infected rats during at least the initial stages of compensatory hyperphagia. This suggests that animals detect a state of energy deficit during the early stages of the infection, yet do not feed, but become hyperphagic coincident with worm loss. The failure of anorectic parasitized animals to feed in response to activation of the NPYergic system makes this a novel system in which to study the regulation of hypothalamic NPY by physiological challenge. There were no significant differences in CRF gene expression between the groups at any of the sampling intervals.
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PMID:Anorexia induced by the parasitic nematode, Nippostrongylus brasiliensis: effects on NPY and CRF gene expression in the rat hypothalamus. 874 24

We have attempted to provide a progress report on current research on the role of catecholamines and serotonin receptor subtypes in feeding control. Recent evidence suggests that only some of the several catecholamine receptor subtypes are specifically involved in feeding control. They include the beta 1/2-adrenoceptors, the alpha 1-adrenoceptors and the D1 dopamine receptors: stimulation of these receptors reduces feeding in rats. Stimulation of serotonergic 5-HT1B and 5-HT2C receptors reduces feeding and perhaps enhances the satiating effect of food. Recently, an interesting reciprocal relation between serotonin and cholecystokinin has been discovered in relation to feeding control. The serotonergic 5-HT2A receptors are involved in stress-induced anorexia and regulate the hyperphagia induced by neuropeptide Y in the nucleus paraventricularis of the hypothalamus. Both effects may involve changes in the secretion of corticotropin-releasing factor. These findings may help elaborate neuronal models of feeding control and perhaps facilitate progress in the pharmacotherapy of human obesity and eating disorders.
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PMID:Pharmacology of ingestive behaviour. 876 44

In order to understand the psychopathology of severe anorexia nervosa (AN), and determine appropriate therapeutic approaches, a clinical study was conducted on 13 patients with severe AN who were hospitalized and were treated with intravenous hyperalimentation (IVH). The patients were divided into three types based on their clinical symptoms and initiating factors: Type I (Restricting Type; "Non-dieters"), Type II (Restricting Type: "Dieters"). Type III (Binge-eating/Purging Type). The clinical features of each type were evaluated. Based on this evaluation, the basic approach and the role of IVH in the treatment of each type are described as follows. Type I: The patients experience loss of appetite and subsequently, suffer involuntary weight loss as a result of psychological or physical stresses at school and/or home. Since the patients do not intentionally restrict food intake, they cannot explain the loss of appetite. The age at onset of this type is the youngest among the three groups. The patients are introverted, passive and not good at expressing their emotions. Therefore, it is often difficult to deepen the emotional commitment further. It is possible to understand the pathology of Type I through the psychosomatic model. IVH therapy promotes benign regression for Type I patients, so that the mother-child relationship may be restored. As the therapeutic progress, the mother child relationship occasionally become ambivalent. In such a case, it is important for the treatment team to support independent activities of the patients. Type II: The patients lose weight by intentionally restricting necessary food intake for reasons such as beauty or sports. Any experience of failure in studies or sports or trouble in complex personal relations can trigger the onset of AN. Weight loss is looked as a great achievement, whereas weight gain is recognized as a serious failure of self-control. Since type II patients understand the necessity of receiving treatment, it is possible to establish a trusting relationship during therapy. Their prognosis is generally good. The psychotherapeutic approach for Type II patients is most effective in the context of a weight gain program utilizing behavior therapy. It is important for the therapist to integrate psychological approach with physiological approach using IVH, and to modify cognitive distortion and body image disturbance. Type III: The patients have regularly engaged in binge eating or purging (or both) in the progress of AN. But as they intensely fear becoming fat, they refuse to maintain a minimally normal body weight. Therefore, they exhibit recurrently inappropriate compensatory behavior in order to prevent weight gain. In the therapeutic sessions, they often become ambivalent and unstable, showing dissatisfaction and reacting strongly against their therapists. The age at onset is the oldest of the three types. The prognosis is not good in many cases. IVH therapy may be required only in life-threatening situation for Type III patients. And severe bulimic patients may require sufficient drug treatment. The patients should be trained for interpersonal relationships at the day care unit or the occupational therapy unit. And they should be encouraged to adapt to real life.
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PMID:[Clinical study of severe anorexia nervosa: the role of intravenous hyperalimentation therapy]. 917 Sep 82

A report is presented of five aged patients with hemorrhagic colon ulcer, which was strongly suspected to be a side effect of non steroidal anti-inflammatory drugs (NSAID). All patients were suffering from orthopedic diseases and NSAIDs were administered for pain: Zaltoprofen for one patient and slow-releasing diclofenac for the other four. Four patients had being treated underlying diabetes mellitus and three of them were being treated with sulfonylurea. Appetite loss was the earliest symptom, 1-2 weeks after administration of NSAID began. Diarrhea occurred 1-2 weeks after appetite loss, and finally hemorrhagic stool developed 1-2 weeks after that. Acute gastric mucosal lesion, hemorrhagic colon ulcer and colitis were diagnosed in all patients by emergency gastro-duodenocolonoscopy. NSAID and oral diet were ceased, and intravenous hyperalimentation was instituted when the patients revealed severe anemia due to bleeding. All patients could take an oral diet after a few weeks. In conclusion hemorrhagic colon ulcer must be prevented in patients treated with NSAID especially those who are aged and have a history of diabetes mellitus.
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PMID:[Hemorrhagic colon ulcer as a side effect of non-steroidal anti-inflammatory drugs in five aged patients]. 943 Sep 88

We have isolated a stable, transplantable, and small glucagonoma (MSL-G-AN) associated with abrupt onset of severe anorexia occurring 2-3 wk after subcutaneous transplantation. Before onset of anorexia, food consumption is comparable to untreated controls. Anorexia is followed by adipsia and weight loss, and progresses rapidly in severity, eventually resulting in reduction of food and water intake of 100 and 80%, respectively. During the anorectic phase, the rats eventually become hypoglycemic and hypothermic. The tumor-associated anorexia shows no sex difference, and is not affected by bilateral abdominal vagotomy, indicating a direct central effect. The adipose satiety factor leptin, known to suppress food intake by reducing hypothalamic neuropeptide Y (NPY) levels, was not found to be expressed by the tumor, and circulating leptin levels were reduced twofold in the anorectic phase. A highly significant increase in hypothalamic (arcuate nucleus) NPY mRNA levels was found in anorectic rats compared with control animals. Since elevated hypothalamic NPY is among the most potent stimulators of feeding and a characteristic of most animal models of hyperphagia, we conclude that the MSL-G-AN glucagonoma releases circulating factor(s) that overrides the hypothalamic NPY-ergic system, thereby eliminating the orexigenic effect of NPY. We hypothesize a possible central role of proglucagon-derived peptides in the observed anorexia.
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PMID:Transplantable rat glucagonomas cause acute onset of severe anorexia and adipsia despite highly elevated NPY mRNA levels in the hypothalamic arcuate nucleus. 943 24

Developed a rating scale to measure body image satisfaction and eating behaviors and disturbances in preadolescent girls and evaluated the psychometric properties of the instrument. The Eating Behaviors and Body Image Test (EBBIT) for preadolescent girls was administered to 291 fourth-, fifth-, and sixth-grade girls to identify the measure's factor structure. Body Image Silhouettes (BIS; Childress, Brewerton, Hodges, & Jarrell, 1993) were also administered, and height and weight measurements were obtained. Although four factors were predicted (maladaptive thoughts about body size, restrictive eating, bingeing, and compensatory behavior for overeating), corresponding to adult criteria for the diagnoses of anorexia and bulimia, factor analysis of the EBBIT suggested only two factors: Body Image Dissatisfaction/Restrictive Eating and Binge Eating Behaviors. Only two compensatory behaviors (exercising to burn off food eaten and skipping meals after overeating) loaded on the scale, and they loaded on the Body Image Dissatisfaction/Restrictive Eating factor. Internal consistency and test-retest reliabilities were adequate to good, and initial validity of the scale was established by using scores on the Body Image Silhouettes, body mass index ratios, age, and race as predictors of EBBIT scores.
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PMID:Underlying dimensions and psychometric properties of the Eating Behaviors and Body Image Test for preadolescent girls. 956 44

The anorexia (anx) mutation causes reduced food intake in preweanling mice, resulting in death from starvation within 3-4 weeks. In wild-type rodents, starvation induces increased neuropeptide Y (NPY) mRNA levels in the arcuate nucleus that promotes compensatory hyperphagia. Despite severely decreased body weight and food intake at 3-weeks age, anx/anx mice do not show elevated NPY mRNA levels in the hypothalamic arcuate nucleus compared to wild-type/heterozygous littermates. The NPY mRNA levels can be upregulated in normal mice at this chronological age, because 24-h food deprivation increased arcuate NPY mRNA in wild-type littermates. The unresponsiveness of NPY expression in the arcuate of anx/anx mice was paralleled by serotonergic hyperinnervation of the arcuate nucleus, comparable to the serotonergic hyperinnervation previously reported in the rest of the anx/anx brain. This result is consistent with the hypothesis that wasting disorders are accompanied by disregulation of NPY mRNA expression in the arcuate nucleus, and suggests that reduced food intake, the primary behavioral phenotype of the anx/anx mouse, may be the result of altered hypothalamic mechanisms that normally regulate feeding.
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PMID:Neuropeptide Y mRNA and serotonin innervation in the arcuate nucleus of anorexia mutant mice. 959 28


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