PMID- 10803799
OWN - NLM
STAT- MEDLINE
DCOM- 20000712
LR  - 20221207
IS  - 0362-5664 (Print)
IS  - 0362-5664 (Linking)
VI  - 23
IP  - 2
DP  - 2000 Mar-Apr
TI  - Neuropharmacology of paradoxic weight gain with selective serotonin reuptake 
      inhibitors.
PG  - 90-7
AB  - It has been suggested that weight gain associated with tricyclic antidepressants 
      (TCA) reflect actions on dopamine (DA) and histamine receptors. However, a 
      definitive cause is purely assumptive given the nonselective pharmacology of 
      these agents. The selective serotonin reuptake inhibitors (SSRIs), as well as 
      agents like dexfenfluramine (DFF), have emphasized the pivotal role of serotonin 
      (5HT) in reducing carbohydrate (CHO) intake, and have provided a more selective 
      tool with which to study appetite regulation. It would be expected that all SSRIs 
      should exert a similar anorectic action. However, recent reports provide evidence 
      to the contrary. Despite their claimed selectivity, SSRIs still interact, either 
      directly or indirectly, with various critical neurotransmitter systems. In 
      addition, although the anorectic action of fluoxetine (FLX) is well recognized, 
      long-term follow-up studies in depressed patients and in obese nondepressed 
      patients reveal that its weight-reducing effects are transient, even leading to a 
      gain in body weight. Similarly, paroxetine (PRX) and citalopram (CTP) have also 
      been associated with weight gain. These latter observations are unexpected 
      because PRX and CTP are highly potent and selective SSRIs. A neuropharmacologic 
      rationale for the apparent paradoxic effects of SSRIs on appetite not a review of 
      neuronal regulation of appetite is presented in this article. As with the 
      regulation of feeding, paradoxic weight gain observed with SSRIs appears to rest 
      on the interaction of 5HT with multiple mechanisms, with the extent of weight 
      gain observed being dependent on subtle, yet important pharmacologic differences 
      within the group. Finally, the neurobiology of depressive illness itself, and of 
      recovery from it, is a major contributing factor to individual response to these 
      drugs.
FAU - Harvey, B H
AU  - Harvey BH
AD  - Department of Pharmacology, Potchefstroom University for Christian Higher 
      Education, South Africa.
FAU - Bouwer, C D
AU  - Bouwer CD
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Clin Neuropharmacol
JT  - Clinical neuropharmacology
JID - 7607910
RN  - 0 (Receptors, Neurotransmitter)
RN  - 0 (Serotonin Uptake Inhibitors)
SB  - IM
MH  - Appetite/drug effects
MH  - Humans
MH  - Receptors, Neurotransmitter/drug effects/metabolism
MH  - Selective Serotonin Reuptake Inhibitors/*adverse effects
MH  - Weight Gain/*drug effects
RF  - 87
EDAT- 2000/05/10 09:00
MHDA- 2000/07/15 11:00
CRDT- 2000/05/10 09:00
PHST- 2000/05/10 09:00 [pubmed]
PHST- 2000/07/15 11:00 [medline]
PHST- 2000/05/10 09:00 [entrez]
AID - 10.1097/00002826-200003000-00006 [doi]
PST - ppublish
SO  - Clin Neuropharmacol. 2000 Mar-Apr;23(2):90-7. doi: 
      10.1097/00002826-200003000-00006.