{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lee SX"],"funding":["NIDDK NIH HHS","NHLBI NIH HHS","NIH"],"pagination":["1615-1626"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5873864"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["128(4)"],"pubmed_abstract":["Insulin resistance and type 2 diabetes are associated with low levels of high-density lipoprotein cholesterol (HDL-C). The insulin-repressible FoxO transcription factors are potential mediators of the effect of insulin on HDL-C. FoxOs mediate a substantial portion of insulin-regulated transcription, and poor FoxO repression is thought to contribute to the excessive glucose production in diabetes. In this work, we show that mice with liver-specific triple FoxO knockout (L-FoxO1,3,4), which are known to have reduced hepatic glucose production, also have increased HDL-C. This was associated with decreased expression of the HDL-C clearance factors scavenger receptor class B type I (SR-BI) and hepatic lipase and defective selective uptake of HDL cholesteryl ester by the liver. The phenotype cou"],"journal":["The Journal of clinical investigation"],"pubmed_title":["FoxO transcription factors are required for hepatic HDL cholesterol clearance."],"pmcid":["PMC5873864"],"funding_grant_id":["F31 HL132484","R01 HL125649","P30 DK026687","R35 HL135833","HL125649","T32 DK007328","T32 DK007647"],"pubmed_authors":["Schlein C","Liu J","Haimi I","Heeren J","Heine M","Fischer AW","Rinninger F","Lee SX","Belnavis G","Ginsberg HN","Ramakrishnan R","Haeusler RA"],"additional_accession":[]},"is_claimable":false,"name":"FoxO transcription factors are required for hepatic HDL cholesterol clearance.","description":"Insulin resistance and type 2 diabetes are associated with low levels of high-density lipoprotein cholesterol (HDL-C). The insulin-repressible FoxO transcription factors are potential mediators of the effect of insulin on HDL-C. FoxOs mediate a substantial portion of insulin-regulated transcription, and poor FoxO repression is thought to contribute to the excessive glucose production in diabetes. In this work, we show that mice with liver-specific triple FoxO knockout (L-FoxO1,3,4), which are known to have reduced hepatic glucose production, also have increased HDL-C. This was associated with decreased expression of the HDL-C clearance factors scavenger receptor class B type I (SR-BI) and hepatic lipase and defective selective uptake of HDL cholesteryl ester by the liver. The phenotype cou","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Apr","modification":"2025-04-26T03:38:51.271Z","creation":"2019-03-26T23:44:12Z"},"accession":"S-EPMC5873864","cross_references":{"pubmed":["29408809"],"doi":["10.1172/JCI94230","10.1172/jci94230"]}}