{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Jiang B"],"funding":["Major Basic Research Project of the Natural Science Foundation of the Jiangsu Higher Education Institutions","National Natural Science Foundation of China","Natural Science Research of Jiangsu Higher Education Institutions of China"],"pagination":["101462"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8938331"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["59"],"pubmed_abstract":["<h4>Objective</h4>Chronic inflammatory response plays a prominent role in obesity-related nonalcoholic fatty liver disease (NAFLD). However, the intrahepatic triggering mechanism of inflammation remains obscure. This study aimed to elucidate the role of serum amyloid A1 (SAA1), an acute-phase response protein, in the obesity-induced hepatic inflammation and NAFLD.<h4>Methods</h4>Male mice were fed a high fat diet (HFD) for 16 weeks, and insulin resistance, hepatic steatosis, and inflammation in mice were monitored. Murine SAA1/2 was genetically manipulated to investigate the role of SAA1 in NAFLD.<h4>Results</h4>We found that SAA1 was increased in the NAFLD liver in both humans and mice. Knockout of SAA1/2 or knockdown of hepatic SAA1/2 promoted energy expenditure and alleviated HFD-induce"],"journal":["Molecular metabolism"],"pubmed_title":["Serum amyloid A1 exacerbates hepatic steatosis via TLR4-mediated NF-κB signaling pathway."],"pmcid":["PMC8938331"],"funding_grant_id":["20KJA310007","81830011","18KJA310003","81870371","82070457","81770417","82030012","82100433","81670263"],"pubmed_authors":["Chen Q","Hu Y","Ben J","Wang D","Zhang H","Li W","Yang X","Li X","Jiang B","Zhu X","Yang Q","Bai H","Liu F"],"additional_accession":[]},"is_claimable":false,"name":"Serum amyloid A1 exacerbates hepatic steatosis via TLR4-mediated NF-κB signaling pathway.","description":"<h4>Objective</h4>Chronic inflammatory response plays a prominent role in obesity-related nonalcoholic fatty liver disease (NAFLD). However, the intrahepatic triggering mechanism of inflammation remains obscure. This study aimed to elucidate the role of serum amyloid A1 (SAA1), an acute-phase response protein, in the obesity-induced hepatic inflammation and NAFLD.<h4>Methods</h4>Male mice were fed a high fat diet (HFD) for 16 weeks, and insulin resistance, hepatic steatosis, and inflammation in mice were monitored. Murine SAA1/2 was genetically manipulated to investigate the role of SAA1 in NAFLD.<h4>Results</h4>We found that SAA1 was increased in the NAFLD liver in both humans and mice. Knockout of SAA1/2 or knockdown of hepatic SAA1/2 promoted energy expenditure and alleviated HFD-induce","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 May","modification":"2025-04-04T08:53:28.589Z","creation":"2025-04-04T08:53:28.589Z"},"accession":"S-EPMC8938331","cross_references":{"pubmed":["35247611"],"doi":["10.1016/j.molmet.2022.101462"]}}