<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>20(20)</volume><submitter>Chen J</submitter><pubmed_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 postna</pubmed_abstract><journal>International journal of molecular sciences</journal><pagination>E5115</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6830345</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>The Potential of the FSP1cre-Pparb/d-/- Mouse Model for Studying Juvenile NAFLD.</pubmed_title><pmcid>PMC6830345</pmcid><pubmed_authors>Wahli W</pubmed_authors><pubmed_authors>Tan NS</pubmed_authors><pubmed_authors>Chen J</pubmed_authors><pubmed_authors>Sng MK</pubmed_authors><pubmed_authors>Zhuang Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>The Potential of the FSP1cre-Pparb/d-/- Mouse Model for Studying Juvenile NAFLD.</name><description>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 postna</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Oct</publication><modification>2025-04-18T17:13:53.572Z</modification><creation>2020-05-21T19:03:42Z</creation></dates><accession>S-EPMC6830345</accession><cross_references><pubmed>31618976</pubmed><doi>10.3390/ijms20205115</doi></cross_references></HashMap>