Fluoxetine Decreases the Proliferation and Adipogenic Differentiation of Human Adipose-Derived Stem Cells
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Updated: Apr 6, 2026
Generation of Human Adipose Stem Cells through Dedifferentiation of Mature Adipocytes in Ceiling Cultures
Published on: March 7, 2015
Bo Kyung Sun1, Ji Hye Kim2,3, Joon-Seok Choi4
1College of Pharmacy, Yonsei University, Incheon 406-840, Korea. bksun2011@gmail.com.
Abstract:
Fluoxetine was originally developed as an antidepressant, but it has also been used to treat obesity. Although the anti-appetite effect of fluoxetine is well-documented, its potential effects on human adipose-derived stem cells (ASCs) or mature adipocytes have not been investigated. Therefore, we investigated the mechanisms underlying the inhibitory effects of fluoxetine on the proliferation of ASCs. We also investigated its inhibitory effect on adipogenic differentiation. Fluoxetine significantly decreased ASC proliferation, and signal transduction PCR array analysis showed that it increased expression of autophagy-related genes. In addition, fluoxetine up-regulated SQSTM1 and LC3B protein expression as detected by western blotting and immunofluorescence. The autophagy inhibitor, 3-methyladenine (3-MA), significantly attenuated fluoxetine-mediated effects on ASC proliferation and SQSTM1/LC3B expression. In addition, 3-MA decreased the mRNA expression of two autophagy-related genes, beclin-1 and Atg7, in ASCs. Fluoxetine also significantly inhibited lipid accumulation and down-regulated the levels of PPAR-γ and C/EBP-α in ASCs. Collectively, these results indicate that fluoxetine decreases ASC proliferation and adipogenic differentiation. This is the first in vitro evidence that fluoxetine can reduce fat accumulation by inhibiting ASC proliferation and differentiation.
Insights
Fluoxetine inhibits human stem cell proliferation and fat cell differentiation by promoting autophagy. This study provides the first in vitro evidence of fluoxetine
Area of Science:
- Biomedical Science
- Cell Biology
- Pharmacology
Background:
- Fluoxetine, an antidepressant, is also used for obesity treatment.
- Its anti-appetite effects are known, but impacts on stem cells are unexplored.
Purpose of the Study:
- Investigate fluoxetine's effects on adipose-derived stem cells (ASCs) proliferation.
- Examine fluoxetine's impact on adipogenic differentiation.
- Elucidate the mechanisms behind fluoxetine's effects on ASCs.
Main Methods:
- Utilized signal transduction PCR array analysis to identify gene expression changes.
- Employed western blotting and immunofluorescence to detect protein levels.
- Assessed lipid accumulation and key adipogenic markers (PPAR-γ, C/EBP-α).
- Used an autophagy inhibitor (3-methyladenine) to confirm the role of autophagy.
Main Results:
- Fluoxetine significantly reduced ASC proliferation and lipid accumulation.
- Increased expression of autophagy-related genes (SQSTM1, LC3B) was observed.
- Autophagy inhibition by 3-methyladenine reversed fluoxetine's effects.
- Fluoxetine down-regulated PPAR-γ and C/EBP-α levels, inhibiting adipogenesis.
Conclusions:
- Fluoxetine inhibits human ASC proliferation and adipogenic differentiation.
- Autophagy plays a key role in fluoxetine's mechanism of action.
- This study offers in vitro evidence for fluoxetine's potential in reducing fat accumulation.
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