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

A boy 14 years of age, weighing 93,45 kg and 143 cm in height was refered to our clinic with hyperphagia and pain in the joints. The patient showed the Prader-Labhart-Willi-syndrome. Through maximal diet therapy, 2 admittances in our ward and through intensive psychological outpatient care, we have seen a weight loss of 26 kg in 18 months and clear improvement in the patient's health. We would like to draw attention to the fact that a weight reduction diet is a cooperative family effort. To satiate uncontrollable hunger an intermittent dose of Fenfluramine (0,5 mg/kg) is recommended.
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PMID:[Treatment of extreme obesity in a case of Prader-Willi-Labhart-syndrome (author's transl)]. 125 Jun 28

(+)-Fenfluramine and (+)-amphetamine have been compared for their ability to reduce food intake in food-deprived rats or eating caused by injecting neuropeptide-Y in the paraventricular hypothalamus of free feeding rats. (+)-Fenfluramine at doses ranging from 0.625 to 5 mg kg-1 reduced eating caused by neuropeptide-Y more effectively than it did the food intake of food-deprived rats, whereas (+)-amphetamine (dose range 0.625-2.5 mg kg-1) reduced both types of eating to a similar extent. The results confirm that (+)-fenfluramine, although less potent than (+)-amphetamine in reducing eating by food-deprived rats, markedly reduces overeating caused by various endogenous substances or stress in free feeding rats. The physiological significance of the neuropeptide-Y-induced eating and its control by (+)-fenfluramine remains to be elucidated.
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PMID:Eating caused by neuropeptide-Y injection in the paraventricular hypothalamus: response to (+)-fenfluramine and (+)-amphetamine in rats. 289 14

The capacity of serotoninergic drugs to selectively suppress carbohydrate (CHO) intake was investigated using a procedure sensitive to drug action. The drug d-fenfluramine was administered chronically to rats whose weight had been increased by exposure to either a fat or CHO-supplemented hyperphagia-inducing diet. The drug exerted a more potent anorexic effect and weight-reducing action in rats given the dietary supplements than in control chow-fed rats. Tolerance to the drug was not apparent even after 40 days of treatment. However, there was no evidence for a selective inhibition of CHO intake, nor was the drug more potent with the CHO-supplemented diet. d-Fenfluramine was equally effective against the hyperphagia and weight gain induced by either fat or CHO supplements.
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PMID:Do serotoninergic drugs decrease energy intake by reducing fat or carbohydrate intake? Effect of d-fenfluramine with supplemented weight-increasing diets. 325 67

Injections of 5,7-dihydroxytryptamine in the nucleus raphe dorsalis did not significantly modify the eating caused by muscimol (100 ng) injected in the same area of freely fed rats 11 days later. Eating caused by muscimol, like food intake in starved rats, was significantly reduced by phenoxybenzamine (5, 10 and 20 mg/kg i.p.). Penfluridol (2.5 and 5 mg/kg p.o.), a dopamine receptor blocker, markedly reduced muscimol-induced eating, but had no effect on the food intake of starved rats. d-Fenfluramine (2.5 mg/kg i.p.), a releaser of serotonin from nerve terminals, significantly reduced eating in muscimol-injected and starved animals whereas d-amphetamine 1.25 and 2.5 mg/kg i.p. only inhibited the food intake of starved rats. Eating elicited by muscimol injected in the nucleus raphe dorsalis appears to constitute a catecholamine-mediated model of hyperphagia selectively inhibited by agents which increase serotonin transmission.
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PMID:Monoamine involvement in the overeating caused by muscimol injection in the rat nucleus raphe dorsalis and the effects of d-fenfluramine and d-amphetamine. 665 54

d-Fenfluramine (0.63 mg/kg i.p.), a serotonin (5-hydroxytryptamine, 5-HT) releaser and re-uptake inhibitor, reduced the eating caused by neuropeptide Y (235 pmol) injected into the paraventricular nucleus of the hypothalamus. The 5-HT1 and 5-HT2 receptor antagonist metergoline (1.0 and 2.0 mg/kg i.p.) and the 5-HT1A and 5-HT1B receptor antagonist (+/-)-cyanopindolol (3.0 and 8.0 mg/kg s.c.) significantly antagonized the effect of d-fenfluramine. The 5-HT2A and 5-HT2C receptor antagonist mesulergine (0.1 and 0.3 mg/kg s.c.) and the 5-HT2A receptor antagonist ketanserin (2.5 and 5.0 mg/kg i.p.) did not significantly modify the effect, nor did the 5-HT1A and 5-HT1B receptor antagonist (-)-propranolol (20-40 nmol), injected bilaterally into the paraventricular nucleus of the hypothalamus. The results suggest that d-fenfluramine reduces neuropeptide Y's hyperphagia by indirectly stimulating 5-HT1B receptors outside the paraventricular nucleus of the hypothalamus.
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PMID:The 5-HT1B receptor mediates the effect of d-fenfluramine on eating caused by intra-hypothalamic injection of neuropeptide Y. 776 74

d-Fenfluramine is a 5-HT agonist which decreases food intake and excessive carbohydrate intake in humans. A placebo-controlled trial of d-fenfluramine (45 mg/day) was conducted in 43 patients with bulimia nervosa. The patients entered an eight-week trial of medication during which they also received cognitive-behavioural therapy. Treatment response was assessed using food diaries to record eating behaviour, and self-rating questionnaires to measure psychopathology. The drug trial, and a follow-up assessment after a further eight weeks, were completed by 39 patients. Abnormal eating behaviour and psychopathology improved significantly in both the d-fenfluramine and placebo groups during the treatment trial. The study failed to show that the addition of d-fenfluramine affords an advantage over brief psychotherapy alone. Although d-fenfluramine is effective in suppressing the overeating, excessive snacking, and excessive carbohydrate consumption which are frequently found in overweight or obese patients, this study suggests that the drug is not an effective treatment for bulimia nervosa.
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PMID:A placebo-controlled trial of d-fenfluramine in bulimia nervosa. 825 96

Inherited overfeeding and fattiness reduce laying performance in broiler breeder pullets. Although feed restriction is used to compensate for overeating and weight gain, this management practice leads to increases in BW variation, labor cost, and bird stress. Dietary supplementation of anorectic agents, such as fenfluramine, may be an alternative. Anak female prebreeder hens (19 wk of age; n = 10 per group) were treated as follows: daily oral administration of 5, 10, 20, or 40 mg DL-fenfluramine/kg BW or saline with food provided for ad libitum intake or administration of saline and feed restriction. Daily feed intake (FI), laying rate, egg composition, and BW were measured. At 40 wk of age, adipose tissue and ovary weights were measured. Fenfluramine depressed (P < 0.05) BW and FI in a dose-dependent manner, but was less effective in reducing BW than feed restriction. Suppression of FI occurred in two phases: a dynamic phase, coinciding with the rapid growth phase, during which FI declined progressively and a static phase during which FI reached a plateau at a significantly low level until the end of the experimental period. Egg production peaked first in saline-treated hens fed for ad libitum intake, but soon after started to decline. In all fenfluramine-treated and feed-restricted hens, egg production peaked 3 to 4 wk later and remained high until the end of the experiment. There were no differences in egg and egg component weights among the experimental groups. Abdominal adipose tissue weight was reduced by fenfluramine in a dose-related manner, and its weight in the group treated with the highest dose was similar to that of feed-restricted hens. In these two groups, ovarian weight was significantly higher than in the saline-treated hens fed for ad libitum intake, and a small, nonsignificant increase in ovary size was observed in groups treated with the two median doses of fenfluramine. The effect of fenfluramine on egg production was similar to that of feed restriction, but it was not dose-dependent and, thus, not directly related to its leaning effect. In broiler breeder hens, oral fenfluramine may be used for chemical feed restriction and diminution of fattiness without reducing egg production relative to manually feed-restricted hens.
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PMID:Effects of fenfluramine on body weight, feed intake, and reproductive activities of broiler breeder hens. 1062 54

The progressive ratio schedule of operant responding is a well utilised task for assessing the rewarding aspects of abused drugs and natural rewards including food. Interestingly, progressive ratio paradigms have mainly been neglected in the field of animal research in obesity. Among the most widely studied mouse models of obesity is the leptin-deficient ob/ob mouse, characterised by hyperphagia and obesity. To date there are no studies on the behaviour of these mice in progressive ratio responding, thus we sought to validate the utility of the progressive ratio paradigm in obese mice and demonstrate its sensitivity to an anorectic drug challenge. Ob/ob mice and their lean controls were tested in fixed ratio paradigms of different demand, extinction learning, and progressive ratio schedules with linear and exponential increments, followed by an anorectic drug challenge with fenfluramine (5 and 10 mg/kg). Obese animals showed equal fixed ratio-acquisition and -responding for ratios 1 and 3, but displayed lower responding in ratios 6 and 9. Interestingly, obese animals showed equal motivation to respond in progressive ratio schedules. Fenfluramine dose-dependently induced anorectic effects in both genotypes and reduced progressive ratio responding significantly. This study, for the first time, describes motivational food intake in an operant progressive ratio paradigm in ob/ob mice. Leptin deficiency did not alter appetitive learning or motivation in the progressive ratio. The utility and sensitivity of the progressive ratio task for studies on motivational food intake was demonstrated by a challenge with the anorectic agent fenfluramine.
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PMID:Progressive ratio responding in an obese mouse model: Effects of fenfluramine. 2072 62