Abstract
The widely prescribed appetite suppressants D-fenfluramine and fluoxetine not only decrease feeding and body weight but also increase extracellular brain 5-HT. As central injection of 5-HT also decreases feeding, the drugs are often thought to require an increase of 5-HT at receptors in order to exert their hypophagic effect. However, much evidence now suggests that D-fenfluramine and its metabolite D-norfenfluramine can cause hypophagia by acting directly at unspecified 5-HT receptors and at 5-HT2C receptors, respectively, while fluoxetine may act independently of 5-HT receptors. These hypophagias may involve interference with the hyperphagic action of neuropeptide Y.
MeSH terms
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Appetite Depressants / administration & dosage
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Appetite Depressants / pharmacology*
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Appetite Depressants / therapeutic use
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Body Weight / drug effects
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Brain / drug effects
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Brain / metabolism*
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Dopamine Agonists / metabolism
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Dopamine Agonists / pharmacology
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Eating / drug effects*
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Eating / physiology
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Female
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Fenfluramine / administration & dosage
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Fenfluramine / pharmacology*
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Fenfluramine / therapeutic use
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Fluoxetine / administration & dosage
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Fluoxetine / pharmacology*
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Fluoxetine / therapeutic use
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Humans
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Male
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Neuropeptide Y / metabolism
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Receptors, Serotonin / drug effects*
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Receptors, Serotonin / metabolism
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Selective Serotonin Reuptake Inhibitors / administration & dosage
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Selective Serotonin Reuptake Inhibitors / pharmacology
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Selective Serotonin Reuptake Inhibitors / therapeutic use
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Serotonin Agents / administration & dosage
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Serotonin Agents / pharmacology
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Serotonin Agents / therapeutic use
Substances
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Appetite Depressants
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Dopamine Agonists
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Neuropeptide Y
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Receptors, Serotonin
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Serotonin Agents
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Serotonin Uptake Inhibitors
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Fluoxetine
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Fenfluramine