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Updated: Mar 25, 2026

Cell Type-specific Gene Expression Profiling in the Mouse Liver
Published on: September 17, 2019
Rapamycin up-regulates triglycerides in hepatocytes by down-regulating Prox1
Sora Kwon1, Ji-Sook Jeon1, Su Bin Kim1
1Department of Pharmaceutical Engineering, Hoseo University, Asan, 336-795, Republic of Korea.
Rapamycin increases triglycerides by reducing Prox1 expression in liver cells. This study reveals a new mechanism linking mTOR signaling to lipid metabolism via Prox1 regulation.
Area of Science:
- Molecular Biology
- Metabolic Research
Background:
- Prolonged rapamycin use can cause hyperlipidemia, but the mechanism is unclear.
- Prox1, a transcription factor, is involved in tissue development and metabolism.
- The direct role of Prox1 in lipid metabolism is not well understood.
Purpose of the Study:
- To investigate the mechanism by which rapamycin affects lipid metabolism.
- To determine the role of Prox1 in regulating triglyceride levels.
- To explore the link between mTOR signaling, Prox1, and lipid metabolism.
Main Methods:
- HepG2 cells and mice were treated with rapamycin.
- Lipid levels were analyzed using thin-layer chromatography.
- Prox1 expression was assessed via western blotting and siRNA/overexpression systems.
Main Results:
- Rapamycin increased triglyceride levels and decreased Prox1 protein in HepG2 cells and mouse liver.
- Prox1 knockdown exacerbated rapamycin-induced triglyceride increase.
- Prox1 overexpression reversed the triglyceride-elevating effect of rapamycin.
Conclusions:
- Rapamycin elevates triglycerides by down-regulating Prox1 expression in hepatocytes.
- Mammalian target of rapamycin (mTOR) signaling regulates triglycerides by maintaining Prox1 expression.
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