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

We have previously shown that coadministration of the dopamine (DA) agonist phentermine plus the serotonergic agonist fenfluramine suppresses alcohol intake and withdrawal seizures in rats. In the present study, phentermine and the serotonin (5-HT) precursor, 5-hydroxy-L-tryptophan (5-HTP), were administered alone, or in combination, to rats fed on a 6% alcohol-containing diet or an isocaloric control diet. Following a 9-h withdrawal period from the alcohol-containing diet, phentermine enhanced the effects of 5-HTP on both reduction of alcohol withdrawal seizures as well as changes in striatal serotonin. Food intake was monitored for 24 h after drug treatment, and neurochemical measures were examined at various time points. Phentermine alone reduced food intake in all diet conditions, but this anorectic effect was followed by hyperphagia in control rats. Phentermine plus 5-HTP reduced the consumption of the alcohol-containing diet, while its effects on consumption of control diets were mixed. In vivo microdialysis in rat nucleus accumbens revealed that phentermine increased extracellular DA, whereas 5-HTP caused marked elevations in extracellular 5-HT. Coadministration of phentermine and 5-HTP evoked simultaneous elevations in extracellular DA and 5-HT that mirrored the effects of each drug alone. Collectively, these findings show that coadministered phentermine plus 5-HTP is effective in reducing alcohol intake and suppressing alcohol withdrawal seizures. These therapeutic actions may be related to elevations in synaptic DA and 5-HT in critical brain regions.
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PMID:Alterations in alcohol consumption, withdrawal seizures, and monoamine transmission in rats treated with phentermine and 5-hydroxy-L-tryptophan. 1641 45

The homeostatic controls over eating are inextricably linked to the reward aspects of eating. The result is an integrated response that coordinates the internal milieu with the prevailing environment. Thus, appetite, which reflects a complex interaction among the external environment, behavioral profile, and subjective states as well as the storage and metabolism of energy, has an important role in the regulation of energy balance. In the prevailing food environment which offers an abundance of food choices it is likely that the motivation to consume from a wide range of delectable foods plays a greater role in contributing to overeating than in the past when the motivation to eat was largely governed by metabolic need. The response to food-related cues can promote strong desires to eat known as cravings by activating the mesocorticolimbic dopamine neurocircuitry. Cravings are associated with subsequent eating and weight-related outcomes. Being able to control food cravings is a determinant of success at adhering to an energy-restricted diet regimen. Increased understanding of the neurocircuitry of appetite regulation, especially reward-related eating behavior, has provided potential targets for therapeutic anti-obesity agents specifically directed at reward mechanisms. The naltrexone-bupropion combination and lorcaserin, which are both approved by the US Food and Drug Administration (FDA) for long-term weight management, have shown promise in addressing craving-related eating behavior. Phentermine and liraglutide are approved as monotherapies for weight management. Preliminary research suggests that liraglutide, as well as phentermine alone or in combination with lorcaserin, may be effective in targeting food cravings. Food components such as thylakoid membranes have also been shown to influence food cravings. This review explores the concepts related to appetite and reward-induced eating behavior, as well as the pharmacological options and food-derived components that may be used to address food cravings.
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PMID:Reward-Induced Eating: Therapeutic Approaches to Addressing Food Cravings. 2771 59