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 effects of serotonin (5-hydroxytryptamine, 5-HT)(1/2) receptor agonists for 5-HT(1) and 5-HT(2) receptors on dark-phase ingestive behavior were evaluated in 12-h food-deprived, female Wistar rats. The amount of food and water consumed after 1, 2, 6 and 12 h was measured. The following agonists were tested: ipsapirone [preferred 5-HT receptor(s) and dose range in mg/kg, IP: 5-HT(1A) and 3-30, respectively], CP-94,253 (5-HT(1B); 0.3-3), TFMPP (5-HT(1B/2C); 0. 3-10), m-CPP (5-HT(2C/1B); 0.3-10), ORG 37684 (5-HT(2C); 0.3-10), BW 723C86 (5-HT(2B); 3-30) and DOI (5-HT(2A/2C); 0.3-3). Ipsapirone induced hyperphagia during the first hour of food access and hypophagia during the last interval. All other compounds induced dose- and time-dependent hypophagia. m-CPP and TFMPP induced the most marked reduction of food intake and were the only drugs inducing rebound hyperphagia. Except for m-CPP and TFMPP, effects on food intake could generally be dissociated from effects on water intake. The receptor profile of the compounds tested suggests that stimulation of 5-HT(1B), 5-HT(2C), 5-HT(2A) or 5-HT(2B) receptors results in hypophagia. As the less selective agonists were the more potent anorexics, it is suggested that simultaneous activation of these receptors results in synergistic effects on ingestive behavior. Additional antagonism studies are required to ascertain the proposed role of particular 5-HT receptor subtypes in the hypophagic effects of the tested compounds.
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PMID:Effects of serotonin(1/2) receptor agonists on dark-phase food and water intake in rats. 1112 93

Administration of the selective 5-HT(1A) agonist, 8-hydroxy-2(di-n-propylamino)tetralin (8-OHDPAT ), to rats produced increases in food intake in freely fed animals and decreases in food intake in food-deprived animals. Acute pre-treatment with various doses of m-chlorophenylpiperazine (m-CPP, another 5-HT agonist) attenuated 8-OHDPAT-induced increases in food intake in the free-feeding paradigm and enhanced 8- OHDPAT-induced decreases in food intake in the food-deprived paradigm. In the two paradigms, however, neither increases nor decreases in food intake induced by 8-OHDPAT were altered in animals following long- term (21-day) treatment with m-CPP versus saline when animals were challenged with 8-OHDPAT 48 h after the last dose of m-CPP. These findings suggest that long-term m-CPP treatment does not alter the functional sensitivity of 5-HT(1A) receptors located pre-synaptically that mediate hyperphagia or 5-HT(1A) receptors located post-synaptically that mediate decreases in food intake by induction of the serotonin behavioural syndrome.
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PMID:Long-term administration of m-chlorophenylpiperazine to rats does not alter functional sensitivity of either pre-synaptic or postsynaptic 5-HT1A receptors. 2228 66

Biological vulnerability concerning eating disorders can include dysfunction of neurotransmitters such as serotonin, dopamine and norepinephrine that regulate feeding. Studies have shown that all three neurotransmitters, especially serotonergic system, are dysfunctional in eating disorders. Although the satiety-promoting role of the serotonergic system in the control of food intake is well established, there is no current evidence that any selective serotonergic receptor subtype mediates the intake of a specific macronutrient. The role of 5-HT1A and 5-HT2C receptor subtypes on food intake and dietary choices was investigated. 20 groups of male Wistar rats, 8 animals each, were intraperitoneal injected 0.05-4.0 mg/kg buspirone (5-HT1A agonist), 1.0 and 3.0 mg/kg mesulergine (5-HT2C antagonist with dopaminergic properties), 5.0 and 10.0 mg/kg m-chlorophenylpiperazine (m-CPP) (5-HT2C/1B agonist) and combinations of mesulergine with buspirone or m-CPP, as well as buspirone with m-CPP at same doses. One group of rats received 1.0 mg/kg apomorphine (dopamine agonist). Animals were given access to a pair of isocaloric diets (protein, PED, or carbohydrate enriched diet, CED) for 4 hours after drug treatment in a food deprivation schedule. Mesulergine caused hyperphagia accompanied by an increase in both PED and CED intake, with CED intake reversed by m-CPP. Busprirone and m-CPP spared protein intake, with an increase and decrease of CED intake consequently. Buspirone due to its action on 5-HT1A autoreceptors seems to affect diet selection indirectly, since its effect on carbohydrate intake is reversed by m-CPP. 5-HT2C receptor blockade seems to be the most significant reason for increased carbohydrate consumption, rather than the inhibition of serotonin (5-HT) release through the 5-HT1A receptors. Our results suggest that both 5-HT1A and 5-HT2C receptor subtypes are involved in the protein-sparing effect of 5-HT, while the 5-HT2C receptors may have the prominent role on 5-HT induced food and carbohydrate intake suppression. These findings extend our understanding on neurobiological substrate of appetite and contribute to the studies related to new drugs against hyperphagia and other eating disorders, especially those referred to 5-HT2C compounds with agonistic properties.
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PMID:[The role of serotonergic 2C receptors in neurobiology and treatment of eating disorders]. 2246 31