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RSS FeedsIJMS, Vol. 20, Pages 5115: The Potential of the FSP1cre-Pparb/d-/- Mouse Model for Studying Juvenile NAFLD (International Journal of Molecular Sciences)

 
 

15 october 2019 16:03:05

 
IJMS, Vol. 20, Pages 5115: The Potential of the FSP1cre-Pparb/d-/- Mouse Model for Studying Juvenile NAFLD (International Journal of Molecular Sciences)
 


Non-alcoholic fatty liver disease (NAFLD) can progress from steatosis to non-alcoholic steatohepatitis (NASH) characterized by liver inflammation, possibly leading to cirrhosis and hepatocellular carcinoma (HCC). Mice with impaired macrophage activation, when fed a high-fat diet, develop severe NASH. Evidence is mounting that Kupffer cells are implicated. However, it is unknown whether the resident CD68+ or bone marrow-derived CD11b+ Kupffer cells are involved. Characterization of the FSP1cre-Pparb/d−/− mouse liver revealed that FSP1 is expressed in CD11b+ Kupffer cells. Although these cells only constitute a minute fraction of the liver cell population, Pparb/d deletion in these cells led to remarkable hepatic phenotypic changes. We report that a higher lipid content was present in postnatal day 2 (P2) FSP1cre-Pparb/d−/− livers, which diminished after weaning. Quantification of total lipids and triglycerides revealed that P2 and week 4 of age FSP1cre-Pparb/d−/− livers have higher levels of both. qPCR analysis also showed upregulation of genes involved in fatty acid β-oxidation, and fatty acid and triglyceride synthesis pathways. This result is further supported by western blot analysis of proteins in these pathways. Hence, we propose that FSP1cre-Pparb/d−/− mice, which accumulate lipids in their liver in early life, may represent a useful animal model to study juvenile NAFLD.


 
620 viewsCategory: Biochemistry, Biophysics, Molecular Biology
 
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IJMS, Vol. 20, Pages 5114: A Review of Computational Methods for Cervical Cells Segmentation and Abnormality Classification (International Journal of Molecular Sciences)
 
 
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