Fluoxetine-induced hepatic lipid accumulation is mediated by prostaglandin endoperoxide synthase 1 and is linked to elevated 15-deoxy-Δ
15-deoxy-Δ12,14PGJ2 (15d-PGJ2)
fatty acid uptake
fluoxetine
non-alcoholic fatty liver disease (NAFLD)
peroxisome proliferator-activated receptor gamma (PPARG)
prostaglandin
prostaglandin-endoperoxide synthase 1 (PTGS1)
prostaglandin-endoperoxide synthase 2 (PTGS2)
selective serotonin reuptake inhibitor (SSRI)
steatosis
Journal
Journal of applied toxicology : JAT
ISSN: 1099-1263
Titre abrégé: J Appl Toxicol
Pays: England
ID NLM: 8109495
Informations de publication
Date de publication:
06 2022
06 2022
Historique:
received:
13
10
2021
accepted:
17
11
2021
pubmed:
14
12
2021
medline:
20
5
2022
entrez:
13
12
2021
Statut:
ppublish
Résumé
Major depressive disorder and other neuropsychiatric disorders are often managed with long-term use of antidepressant medication. Fluoxetine, an SSRI antidepressant, is widely used as a first-line treatment for neuropsychiatric disorders. However, fluoxetine has also been shown to increase the risk of metabolic diseases such as non-alcoholic fatty liver disease. Fluoxetine has been shown to increase hepatic lipid accumulation in vivo and in vitro. In addition, fluoxetine has been shown to alter the production of prostaglandins which have also been implicated in the development of non-alcoholic fatty liver disease. The goal of this study was to assess the effect of fluoxetine exposure on the prostaglandin biosynthetic pathway and lipid accumulation in a hepatic cell line (H4-II-E-C3 cells). Fluoxetine treatment increased mRNA expression of prostaglandin biosynthetic enzymes (Ptgs1, Ptgs2, and Ptgds), PPAR gamma (Pparg), and PPAR gamma downstream targets involved in fatty acid uptake (Cd36, Fatp2, and Fatp5) as well as production of 15-deoxy-Δ
Substances chimiques
PPAR gamma
0
Fluoxetine
01K63SUP8D
Cyclooxygenase 2
EC 1.14.99.1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1004-1015Informations de copyright
© 2021 John Wiley & Sons, Ltd.
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