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Updated: Mar 23, 2026
Isolation and Differentiation of Adipose-Derived Stem Cells from Porcine Subcutaneous Adipose Tissues
Published on: March 31, 2016
[Overexpression of PPARγ induces adipogenic steatosis in mouse primary hepatocytes]
Liang Bai1, Yali Zhang1, Chen Xie1
1Research Institute of Atherosclerotic Disease, Xi'an Jiaotong University School of Medicine, Xi'an 710061, China;Laboratory Animal Center, Xi'an Jiaotong University School of Medicine, Xi'an 710061, China.
Objective:
To investigate the effects of PPARγ overexpression on steatosis in mouse primary hepatocytes.
Methods:
Primary hepatocytes isolated from C57BL/6J mice were infected with either Ad/LacZ or Ad/PPARγ for 48 h. Steatosis of the primary hepatocytes was checked by Oil Red O staining. The mRNA and protein expression of adipocyte-specific genes PPARγ, aP2 and CideA were analyzed by using RT Real-time PCR and Western Blot.
Results:
Primary hepatocytes were small and even. Hepatocyte nuclei were round with dispersed chromatin and prominent nucleoli. Accumulated lipid droplets were observed in Ad/PPARγ-infected hepatocytes, but in Ad/LacZ-infected hepatocytes. Moreover, compared with Ad/LacZ-infected hepatocytes, the mRNA expression of PPARγ, aP2, FGF21 and CideA in Ad/PPARγ-infected hepatocytes were significantly induced, the protein expression of PPARγ and its target aP2 strongly increased.
Conclusion:
over expression of PPARγ induces adipogenic steatosis in mouse primary hepatocytes.
Insights
Overexpression of peroxisome proliferator-activated receptor gamma (PPARγ) in mouse liver cells induces fat accumulation, a condition known as steatosis. This finding highlights PPARγ
Area of Science:
- Hepatology
- Molecular Biology
- Cell Biology
Background:
- Fatty liver disease (steatosis) is a growing health concern.
- Peroxisome proliferator-activated receptor gamma (PPARγ) is a key regulator of adipogenesis.
- The role of PPARγ in hepatic steatosis requires further elucidation.
Purpose of the Study:
- To investigate the impact of PPARγ overexpression on steatosis in primary mouse hepatocytes.
- To analyze the expression of PPARγ and its target genes in response to PPARγ induction.
Main Methods:
- Primary hepatocytes were isolated from C57BL/6J mice.
- Hepatocytes were infected with adenovirus carrying either LacZ (control) or PPARγ.
- Steatosis was assessed using Oil Red O staining.
- Gene and protein expression were quantified via RT-qPCR and Western Blot.
Main Results:
- PPARγ overexpression led to the accumulation of lipid droplets in hepatocytes.
- Significant induction of mRNA for PPARγ, aP2, FGF21, and CideA was observed.
- Protein levels of PPARγ and its target gene aP2 were markedly increased.
Conclusions:
- PPARγ overexpression promotes adipogenic steatosis in mouse primary hepatocytes.
- This study provides evidence for PPARγ's role in regulating hepatic lipid metabolism.
