Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/142227
Title: The potential of the FSP1cre-Pparb/d-/- mouse model for studying juvenile NAFLD
Authors: Chen, Jiapeng
Zhuang, Yan
Sng, Ming Keat
Tan, Nguan Soon
Wahli, Walter
Keywords: Science::Medicine
Issue Date: 2019
Source: Chen, J., Zhuang, Y., Sng, M. K., Tan, N. S., & Wahli, W. (2019). The potential of the FSP1cre-Pparb/d-/- mouse model for studying juvenile NAFLD. International Journal of Molecular Sciences, 20(20), 5115-. doi:10.3390/ijms20205115
Journal: International Journal of Molecular Sciences
Abstract: 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.
URI: https://hdl.handle.net/10356/142227
ISSN: 1661-6596
DOI: 10.3390/ijms20205115
Rights: © 2019 The Authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:SBS Journal Articles

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