{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Nanizawa E"],"funding":["Merck Sharp & Dohme"],"pagination":["100736"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7021552"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["22"],"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"],"journal":["Biochemistry and biophysics reports"],"pubmed_title":["Short-term high-fat diet intake leads to exacerbation of concanavalin A-induced liver injury through the induction of procoagulation state."],"pmcid":["PMC7021552"],"funding_grant_id":["6100030047"],"pubmed_authors":["Tamaki Y","Hayashi Y","Ishikawa T","Ito H","Miyashita R","Kanbe A","Sono R","Nanizawa E"],"additional_accession":[]},"is_claimable":false,"name":"Short-term high-fat diet intake leads to exacerbation of concanavalin A-induced liver injury through the induction of procoagulation state.","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","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Jul","modification":"2025-04-18T15:50:53.701Z","creation":"2020-05-22T10:44:00Z"},"accession":"S-EPMC7021552","cross_references":{"pubmed":["32083190"],"doi":["10.1016/j.bbrep.2020.100736"]}}