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)

Opiate antagonist inhibition of deprivation-induced intake and 2-deoxy-D-glucose (2DG) hyperphagia is significantly enhanced by the 5-hydroxytryptamine3 (5-HT3) antagonist, ICS-205,930. Interactions between opiate antagonists and either 5-HT or 5-HT2 antagonists produced smaller effects. The present study evaluated whether insulin (5 U/kg) hyperphagia was affected by methysergide (0.5-5 mg/kg), ritanserin (0.25-2.5 mg/kg), and ICS-205,930 (0.5-5 mg/kg) alone or in combination with naltrexone (2.5-10 mg/kg). Whereas ICS-205,930 stimulated insulin hyperphagia across the 6-h time course, ritanserin and, to a lesser degree, methysergide reduced insulin hyperphagia. Naltrexone marginally (19-33%) reduced insulin hyperphagia. Pairing naltrexone with either ICS-205,930 or ritanserin significantly suppressed insulin hyperphagia after 2 h. Pairing naltrexone with each of the serotonin antagonists significantly enhanced insulin hyperphagia after 4 and 6 h. These data suggest that 5-HT2 and 5-HT3 receptor subtypes interact with opioid systems to modulate insulin hyperphagia. Given that central insulin reduces food intake and body weight, the interaction between serotonergic and opioid systems may occur peripherally.
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PMID:Naltrexone, serotonin receptor subtype antagonists, and glucoprivic intake: 2. Insulin. 151 48

Multiple lines of experimental evidence point to the involvement of endogenous opiates in appetite regulation. Post brain injury patients often exhibit driven eating behaviour. Since this problem fails to respond to behaviour modification, appetite suppressants, lithium, or any other usual approach, the use of the oral narcotic antagonist, Naltrexone, was given to three such patients. Naltrexone binds multiple opiate receptor sites in the hypothalamus, including the kappa receptors which have been implicated in appetite regulation, the use of this narcotic antagonist in hypothalamic hyperphagia appears to be a rational approach to this intractable problem. In this open trial, lasting from 4 1/2 to 9 months, the minimal effective dose appeared to be in the range of 100 mg per day. No side-effects (for example elevations in liver enzymes) were noted. All of the patients had an improved sense of well-being and their behaviours were less difficult to manage when on the Naltrexone. The significance of this preliminary trial is that narcotic antagonists may have a role in the treatment of brain-injured patients with bulimia. Also, Naltrexone may be useful in treating other maladaptive behavioural consequences of head trauma such as stealing, manipulation, demandingness, and depression. Likewise, the effects on the deranged endocrine system, such as the hypogonadism, are significant and deserve further exploration.
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PMID:Naltrexone in organic bulimia: a preliminary report. 345 71

The effects of opioid antagonists on seasonal changes in feeding behavior of white-tailed deer (Odocoileus virginianus) during fall, winter, and summer, as well as in bottle-fed fawns are described. Naltrexone had no effect on the amount of milk ingested by bottle-fed fawns. After weaning naltrexone significantly decreased feeding in both the summer and winter, with no difference in the effect for either season, indicating that opioids do not play a role in the winter hypophagia or the summer hyperphagia in deer. Similarly there was no seasonal effect on the ability of naloxone to decrease feeding in yearlings during summer, fall, and winter. Naltrexone significantly decreased spontaneous locomotion in the fawns in winter and the fall. In yearlings there was a tendency for the high dose of naloxone to decrease spontaneous locomotion in winter whereas in summer and fall it tended to enhance time spent moving. These data suggest that the endogenous opioid control of feeding in deer is independent of the seasonal effect on feeding and endogenous opioids do not play a role in the seasonal rhythmicity of feeding in deer. The effects of endogenous opioids on spontaneous locomotion do appear to be linked to changes in seasonal activity patterns.
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PMID:Effects of opiate antagonists on feeding and spontaneous locomotion in deer. 409 90

A highly palatable diet (cafeteria diet) provokes an hyperphagia. The effects of Mu and Kappa opiate antagonists (Mu : Naltrexone 0.5 mg/Kg IP; Kappa Mr2266 0.5; 2.5; 10) and agonists (Mu Morphine 0.05; 0.1; 0.5; 2.5; Kappa Mr2033 0.5; 2.5) were studied on the nocturnal food intake of cafeteria rats and chow rats fed with monotonous food. At low doses Mu as well as Kappa antagonists do not modify the food intake of chow rats, but suppress the hyperphagia induced by the cafeteria diet. Kappa agonist provokes a decrease in food intake in chow and cafeteria rats while the Mu agonist at low doses suppresses the hyperphagia induced by cafeteria diet. The involvement of these two opioid systems in this type of hyperphagia is discussed.
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PMID:Difference in sensitivity of the mu and kappa systems in cafeteria rats. 609 8

Discrete, bilateral, radiofrequency destruction of the ventral noradrenergic bundle (VB) resulted in a pronounced fall in levels of noradrenaline in the hypothalamus but not in the cortex. On days 4 and 12, but not 28, post-surgery, VB-lesioned rats were hyperactive (rearing and ambulation) upon exposure to a novel open-field space. This hyperactivity was greatly attenuated by naloxone, which did not significantly modify sham activity. These data suggest that the VB may be involved in the control of locomotor-exploratory activity via an interaction with an endorphinergic system. On day 4, but not 12 or 25, VB-lesioned rats displayed a significant elevation in core temperature (Tc). No difference in the hyperthermia elicited by introduction into the open-field was, however, seen between VB-lesioned and sham rats on day 4. In both groups, this rise in Tc was strongly attenuated by naloxone. These data indicate that the VB may be involved in the control of Tc but that it does not mediate novelty-stress evoked hyperthermia, for which endorphins are primarily responsible. Within 7 days post-surgery, VB-lesioned rats developed an enhancement of daily food intake which led to a slight obesity. From day 15 onward, a hyperdipsia was also seen in VB-lesioned rats. Naltrexone reduced the food and water intake of both sham and VB-lesioned animals but failed to totally block this hyperphagia. It is suggested that the VB is involved in the regulation of daily ingestive behaviour and that endorphins do not exclusively mediate the VB-lesion induced hyperphagia.
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PMID:The role of the ventral noradrenergic bundle in relation to endorphins in the control of core temperature, open-field and ingestive behaviour in the rat. 683 76

A highly palatable diet (ordinary chow supplemented with 4 highly palatable items changes every day) (HPD) provokes hyperphagia and overweight in the rat. After 17 weeks of such a diet, naltrexone (0.5 or 2.5 mg/kg IP) and opiate antagonist, was injected at the beginning of the dark period, and a food intake test was performed during the 3 following hours. Naltrexone does not modify the energy intake in control rats receiving ordinary chow but suppresses HPD induced hyperphagia. The involvement of the beta-endorphin system in this type of hyperphagia is discussed.
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PMID:Naltrexone suppresses hyperphagia induced in the rat by a highly palatable diet. 729 Dec 35

Functional interactions between serotonergic (5-HT) and opioid drugs have been observed with 5-HT3 receptor antagonism enhancing the inhibitory actions of naloxone and naltrexone in both food-deprived and glucoprivic rats; 5-HT2A/C receptor antagonism enhanced naltrexone's inhibition of insulin hyperphagia. The present study examined whether pretreatment with either general 5-HT (methysergide: 0.5-5 mg/kg), 5-HT2A/C (ritanserin: 0.25-2.5 mg/kg), or 5-HT3 (ICS 205930: 0.5-5 mg/kg) antagonists altered the pattern and magnitude of ad lib intake of simple (sucrose: 10%) or more complex (maltose dextrin: MD, 10%) carbohydrate solutions, or naltrexone's (0.25-2.5 mg/kg) inhibition of these forms of intake. Methysergide significantly increased the pattern and magnitude of sucrose intake at low (0.5-2.5 mg/kg) doses, and transiently delayed the pattern of MD intake at high (5 mg/kg) doses. Ritanserin significantly accelerated the pattern, but not the magnitude of sucrose intake at low (0.25-1.25 mg/kg) doses without affecting MD intake. ICS 205930 reduced the magnitude of sucrose intake at the highest (5 mg/kg) dose, and transiently reduced MD intake. Naltrexone dose dependently altered the pattern and magnitude of both sucrose and MD intake. Coadministration of ritanserin and naltrexone either eliminated or delayed the pattern of opioid antagonist inhibition of both sucrose and MD intake. Methysergide and ICS 205930 pretreatment produced minor changes in the pattern of naltrexone-induced inhibition. These data indicate that 5-HT receptor differentially modulate the pattern of carbohydrate intake, and indicate differential ingestive interactions between 5-HT and opioid antagonists under challenge and palatable conditions.
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PMID:Naltrexone, serotonin receptor subtype antagonists, and carbohydrate intake in rats. 802 91

A 28-year-old woman with acquired brain damage suffered subsequent profound mental disability and an intense hyperphagic syndrome complete with life-threatening pica. She was the single subject of two consecutive experiments. In the first, Naltrexone, an orally administered opiate blocker, was given to reduce hyperphagia and distress, but was associated with even greater urgency when eating meals and a manifest increase in distress. While distress reduced to premedication levels on withdrawal of treatment, urgency of eating did not reduce so quickly. In the second experiment a laser acupuncture procedure was used at 2.5 Hz and 10 Hz for 10 days each with an intervening 10-day placebo condition to increase the availability of the subject's endogenous opiates, and thus hopefully produce opposite effects to the first experiment and effect a positive treatment. The 10 Hz condition produced a significant but transient reduction in pica measured by attempts at pica on a supervised walk shortly after each treatment. The subject was also easier to manage on walks, and appeared happier. Further studies using physical exercise or acupressure to achieve similar or better results are discussed.
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PMID:Reducing naltrexone-resistant hyperphagia using laser acupuncture to increase endogenous opiates. 893 9

Orphanin FQ/nociceptin binds with high affinity to the orphan opioid receptor-like/K-3 (ORL1/KOR-3) clone, and stimulates feeding. The present study demonstrated that antisense oligodeoxynucleotides directed against either exons 1, 2 or 3 of the ORL1/KOR-3 clone reduced orphanin FQ/nociceptin-induced hyperphagia. A missense probe was ineffective. Naltrexone dose-dependently reduced orphanin FQ/nociceptin-induced hyperphagia. These data suggest that the receptor responsible for orphanin FQ/nociceptin-induced hyperphagia is encoded by the ORL1/KOR-3 clone.
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PMID:Orphan opioid receptor antisense probes block orphanin FQ-induced hyperphagia. 966 88

Obese Zucker female rats are hyperphagic, overweight, infertile, and hyporesponsive to the inductive effects of ovarian steroid hormones on sexual behaviors. It has been postulated that endogenous opioid activity may contribute to their obesity and reproductive dysfunction. To test this hypothesis, ovariectomized, adult obese Zucker rats were treated with the opioid receptor antagonist, naltrexone, or saline prior to measurement of steroid-induced sexual behaviors, food intake, and body weight. In estradiol benzoate (EB)-treated rats, naltrexone injection increased the display of sexual receptivity (lordosis quotient, LQ: saline, 11+/-10%; 5 mg/kg naltrexone, 54+/-15%, p < 0.05) and also elicited proceptivity (PRO), which was never observed after saline injection. In EB plus progesterone-treated animals, naltrexone administration enhanced both sexual receptivity and proceptivity (LQ: saline, 17+/-10%; 5 mg/kg naltrexone, 96+/-3%; p < 0.05; PRO: saline, 3.0+/-2.4 bouts/min; 5 mg/kg naltrexone, 45.3+/-12 bouts/min; p < 0.01). Naltrexone injection also decreased 24-h food intake (saline, 24.2+/-0.7 g; 5 mg/kg naltrexone, 17.6+/-1.2 g; p < 0.05) and weight change (saline, +7.3+/-0.8 g; 5 mg/kg naltrexone, -4.5+/-1.4 g, p < 0.01). Morphine treatment blocked these effects of naltrexone on sexual behaviors, food intake, and body weight. These data suggest that endogenous opioids contribute to hyperphagia, obesity, and behavioral hyporesponsiveness to ovarian steroid hormones in obese Zucker rats.
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PMID:Opioid receptor blockade promotes weight loss and improves the display of sexual behaviors in obese Zucker female rats. 1041 95


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