<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Nanizawa E</submitter><funding>Merck Sharp &amp;amp; Dohme</funding><pagination>100736</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7021552</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>22</volume><pubmed_abstract>Obesity and high-fat diet (HFD) are known to cause proinflammatory and procoagulation states and suggested to become a risk of developing thromboembolic diseases. Non-alcoholic fatty liver disease (NAFLD) is usually associated with obesity and HFD, and a part of NAFLD is known to progress to nonalcoholic steatohepatitis (NASH), the pathogenesis of which has not been fully elucidated. In the current study, we examined the influence of short-term HFD on hepatic expression of the molecules related to inflammation, coagulation, metabolism, and cellular stresses from the perspective that HFD itself can be a risk for the development to NASH. In the analysis in short-term (4 days to 14 days) HFD-fed mice, we found out that HFD increased hepatic expression of IFN-γ, TNF-α, IL-10, monocyte chemotac</pubmed_abstract><journal>Biochemistry and biophysics reports</journal><pubmed_title>Short-term high-fat diet intake leads to exacerbation of concanavalin A-induced liver injury through the induction of procoagulation state.</pubmed_title><pmcid>PMC7021552</pmcid><funding_grant_id>6100030047</funding_grant_id><pubmed_authors>Tamaki Y</pubmed_authors><pubmed_authors>Hayashi Y</pubmed_authors><pubmed_authors>Ishikawa T</pubmed_authors><pubmed_authors>Ito H</pubmed_authors><pubmed_authors>Miyashita R</pubmed_authors><pubmed_authors>Kanbe A</pubmed_authors><pubmed_authors>Sono R</pubmed_authors><pubmed_authors>Nanizawa E</pubmed_authors></additional><is_claimable>false</is_claimable><name>Short-term high-fat diet intake leads to exacerbation of concanavalin A-induced liver injury through the induction of procoagulation state.</name><description>Obesity and high-fat diet (HFD) are known to cause proinflammatory and procoagulation states and suggested to become a risk of developing thromboembolic diseases. Non-alcoholic fatty liver disease (NAFLD) is usually associated with obesity and HFD, and a part of NAFLD is known to progress to nonalcoholic steatohepatitis (NASH), the pathogenesis of which has not been fully elucidated. In the current study, we examined the influence of short-term HFD on hepatic expression of the molecules related to inflammation, coagulation, metabolism, and cellular stresses from the perspective that HFD itself can be a risk for the development to NASH. In the analysis in short-term (4 days to 14 days) HFD-fed mice, we found out that HFD increased hepatic expression of IFN-γ, TNF-α, IL-10, monocyte chemotac</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Jul</publication><modification>2025-04-18T15:50:53.701Z</modification><creation>2020-05-22T10:44:00Z</creation></dates><accession>S-EPMC7021552</accession><cross_references><pubmed>32083190</pubmed><doi>10.1016/j.bbrep.2020.100736</doi></cross_references></HashMap>