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)

The effect of estrogen supplement on selective D2 receptor antagonist sulpiride induced weight gain was examined in ovariectomized (ovx.) rats. Sulpiride injection (10 mg/kg, s.c.) showed a significant increase of body weight and food consumption only in female rats. Bilateral ovariectomy completely abolished the weight gain and hyperphagia by sulpiride. Subcutaneous injection of estradiol benzoate (E2:5 micrograms/day, s.c.) for 14 days restored the effects of sulpiride on weight gain in ovx, rats and sulpiride injection with E2 supplement significantly increased the efficiency of food utilization. The present study suggested that estrogen should be involved in the induction of overweight and hyperphagia by sulpiride.
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PMID:Involvement of sex hormone in body weight gain by selective D2 receptor antagonist sulpiride. 227 23

Sulpiride (20 mg/kg/ip for 21 days) induced in female rats a significant body weight increase and hyperphagia. After drug withdrawal a significant hypophagia was observed. It is hypothesised that this hypophagia might be a spontaneous manifestation of D2 dopamine receptors supersensitivity, either in the perifornical region of the lateral hypothalamus or in the pituitary.
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PMID:Hypophagia after long-term administration of sulpiride in adult female rats: a model of D2 dopamine receptors supersensitivity? 252 18

Sulpiride (20 mg/kg, i.p.) for 21 days increased body weight in prepubertal, peripubertal and adult female rats. The increment was higher in the adult group, where a significant hyperphagia was also noted. In males, the same treatment tended to decrease body weight in the peripubertal and adult groups while in the prepubertal animals an increase of body weight without a significant hyperphagia was observed. These results are discussed in terms of an hypothetical sulpiride-induced reduction in serum gonadal steroid levels.
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PMID:Puberty modifies sulpiride effects on body weight in rats. 318 86

Local injection of sulpiride to block dopamine (primarily D2-type) receptors in the perifornical lateral hypothalamus (pf-LH) can induce locomotion, feeding, and drinking, and in the present study, local sulpiride induced reward and dopamine (DA) release in the nucleus accumbens. Sulpiride injected bilaterally (4, 8, and 16 micrograms/0.3 microliters), ipsilaterally, or contralaterally (8 micrograms) in the pf-LH increased extracellular levels of DA and its metabolites in the accumbens. Bilateral sulpiride injected posterior and medial to the pf-LH controlled for diffusion to the ventricle or ventral midbrain. Rats self-injected sulpiride (210 ng/21 nl/2 s) in the pf-LH (111 resp/2 h on drug lever vs. 20 resp on a blank lever). Thus, cells in the pf-LH establish connections with mesolimbic DA neurons involved in the behavior reinforcement process. Evidently hypothalamic cells with DA receptors normally inhibit aspects of behavior reinforcement. Disinhibition with hypothalamic sulpiride is reward for self-injection and cause of overeating that can lead to obesity.
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PMID:Rats self-inject a dopamine antagonist in the lateral hypothalamus where it acts to increase extracellular dopamine in the nucleus accumbens. 750 63

1. Obesity is an undesirable side effect of neuroleptics which affects 50% approximately of patients under a program of chronic administration. 2. An animal model of neuroleptic-induced obesity and hyperphagia has been developed in female rats treated chronically with sulpiride (20 mg/Kg/ip. for 21 days). However, it is unknown whether or not the hyperphagia is essential for the development of this type of obesity. 3. Sulpiride or vehicle was administered in two experimental conditions: in the first one, food was available in an amount which was three times the previous individual daily food intake; in the second one, the daily food provision was maintained at the individual daily average before starting the treatments. This way hyperphagia was prevented in half of the groups. Besides the body weight gain measurement in all the groups, the serum levels of estradiol, prolactin, glucose and lipids were assessed in the groups with unrestricted food intake. 4. Food restriction prevented the sulpiride-induced weight gain, even though the rats displayed a permanent diestrus which suggests an hyperprolactinemia-induced impairment in the balance of the reproductive hormones that may promote weight gain. However, the basal levels of estradiol were not affected by sulpiride. 5. The high density cholesterol was significantly increased by sulpiride, and the serum glucose levels were significantly decreased, however these changes were only detected during the first week of treatment. 6. The decrease in the serum glucose levels may be an early consequence of hyperinsulinemia. 7. Neuroleptic-induced obesity in rats appears to mimic energy intake, endocrine status and carbohydrate metabolism in humans under chronic neuroleptic administration. However, these rodents did not display the typical changes in blood lipids observed in human obesity.
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PMID:Mechanism of the neuroleptic-induced obesity in female rats. 953 75

Sulpiride (SUL, 20 mg kg-1 day-1) induces weight gain, hyperphagia, hyperprolactinemia, hypogonadism, and perhaps increased insulin sensitivity in rats. Leptin seems to signal the brain about the size of body fat stores and nutrient metabolism. We evaluated the basal serum leptin levels in rats after acute (1 h) or prolonged SUL or vehicle administration (10, 20 and 30 days). At days 10 and 30 leptin was also assessed during a glucose overload test. As the maximal weight gain during SUL administration is observed at days 10-15 of treatment, leptin was measured in a comparison group of insulin-treated rats (5 IU day-1 for 10 days). SUL-treated rats significantly gained weight. However, leptin levels were not significantly increased at any time-point of treatment. SUL did not affect insulin levels either. By contrast, leptin levels were significantly elevated after insulin administration, along with weight gain and hyperinsulinemia. An opposite correlation was also observed at day 10: leptin and insulin correlated negatively in the SUL group and positively in the insulin group. In addition, leptin and the magnitude of weight gain tended to correlate positively after SUL treatment, but negatively after insulin administration. SUL-treated rats, thus, appear to exhibit an unusual type of weight gain, characterized by normal circulating leptin and insulin levels. Such a particular leptin profile may be related to hyperprolactinemia, hypogonadism or lack of hyperinsulinemia. Molecular Psychiatry (2000) 5, 70-76.
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PMID:Antipsychotic drug-induced obesity in rats: correlation between leptin, insulin and body weight during sulpiride treatment. 1067 71