Neurochemical mechanism of action of drugs which modify feeding via the serotoninergic system
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Cited by (187)
Fenfluramine repurposing from weight loss to epilepsy: What we do and do not know
2021, Pharmacology and TherapeuticsCitation Excerpt :In the same experimental system, d-fenfluramine and d-norfenfluramine also released noradrenaline, whereas l-fenfluramine did not affect noradrenaline release and l-norfenfluramine was weakly active (Rothman, Clark, Partilla, & Beumann, 2003). The release of 5-HT induced by d-fenfluramine is preferentially exocytotic while norfenfluramine mainly acts on the non-vesicular pool (Garattini et al., 1986). Although both fenfluramine enantiomers and their metabolites have no major effects on dopaminergic mechanisms in vitro, l-fenfluramine and l-norfenfluramine have several biochemical and behavioral effects typical of antipsychotic drugs in experimental models, suggesting that they may control dopamine transmission in vivo (Bendotti, Borsini, Zanini, Samanin, & Garattini, 1980; Bettini, Ceci, Spinelli, & Samanin, 1987; Garattini et al., 1986; Invernizzi, Berettera, Garattini, & Samanin, 1986; Invernizzi, Bertorelli, Consolo, Garattini, & Samanin, 1989; Rothman et al., 2003).
Role of the serotonergic system in appetite and ingestion control
2020, Handbook of Behavioral NeuroscienceCitation Excerpt :Blundell's seminal review (Blundell, 1977), which became a citation classic, synthesized these early studies and proposed that endogenous serotonin inhibits food consumption by augmenting short-term satiety processes during both a meal and the subsequent postingestive period. Much of our understanding of the role of the serotonergic system in the control of appetite and ingestive behavior has developed from studies carried out between the 1970s and early 1990s using the serotonin releaser and reuptake inhibitor fenfluramine (Garattini et al., 1986, 1987), initially with the racemic dl-fenfluramine and later the more potent isomer d-fenfluramine. In fact, until 1997 when fenfluramine was withdrawn as an antiobesity treatment due to its association with valvular heart disease (Connolly et al., 1997), it was the prototypical compound for investigating serotonergic mechanisms underpinning food intake and satiety.
Lorcaserin: A review of its preclinical and clinical pharmacology and therapeutic potential
2020, Pharmacology and TherapeuticsNew therapeutic opportunities for 5-HT<inf>2</inf> receptor ligands
2017, Pharmacology and TherapeuticsCitation Excerpt :However, clinical use of DF has been associated with several unacceptable side effects including primary pulmonary hypertension and valvular heart disease (Fitzgerald et al., 2000; Rothman et al., 2000; Launay et al., 2002), and this anorexigen was withdrawn from the market in 1997. In the early 1980s, Mennini and colleagues performed pioneering work initially describing the effect of DF and derivatives on the release of 5-HT into nerve terminals by targeting the serotonin transporter (SERT) (Garattini et al., 1986). Administration of DF suppresses food intake in both animals and humans.
Mechanisms linking depression co-morbid with obesity: An approach for serotonergic type 3 receptor antagonist as novel therapeutic intervention
2015, Asian Journal of PsychiatryCitation Excerpt :Human studies confined the suppression of intake of highly palatable high fat foods and a possible avoidance of fat after the administration of dexfenfluramine and sumatriptan (Blundell and Halford, 1998). The role of serotonin in the regulation of the food intake has been explored in several earlier studies (Blundell et al., 1984; Garattini et al., 1986). Serotonin release or uptake inhibitor, fenfluramine is reported to inhibit food intake in both animals (Duhault et al., 1975) and humans (Silverstone and Goodall, 1986).
Serotonin controlling feeding and satiety
2015, Behavioural Brain Research