{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ouyang S"],"funding":["National Natural Science Foundation of China"],"pagination":["e2401311"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11633478"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(46)"],"pubmed_abstract":["Glycerol kinase (GK) participates in triglyceride (TG) synthesis by catalyzing glycerol metabolism. Whether GK contributes to nonalcoholic fatty liver (NAFL) is unclear. The expression of hepatic Gk is found to be increased in diet-induced and genetic mouse models of NAFL and is positively associated with hepatic SREBP-1c expression and TG levels. Cholesterol and fatty acids stimulate GK expression in hepatocytes. In HFD-induced NAFL mice, knockdown of hepatic Gk decreases expression of SREBP-1c and its target lipogenic genes as well as DGAT1/2, increases serum glycerol levels, decreases serum TG levels, and attenuates hepatic TG accumulation. Overexpression of GK in hepatocytes in mice or in culture produces opposite results. Mechanistic studies reveal that GK stimulates SREBP-1c transcri"],"journal":["Advanced science (Weinheim, Baden-Wurttemberg, Germany)"],"pubmed_title":["Glycerol Kinase Drives Hepatic de novo Lipogenesis and Triglyceride Synthesis in Nonalcoholic Fatty Liver by Activating SREBP-1c Transcription, Upregulating DGAT1/2 Expression, and Promoting Glycerol Metabolism."],"pmcid":["PMC11633478"],"funding_grant_id":["32071153"],"pubmed_authors":["Ouyang S","Li Y","Yu S","Le Y","Yang M","Ying H","Zhu T","Zhuo S"],"additional_accession":[]},"is_claimable":false,"name":"Glycerol Kinase Drives Hepatic de novo Lipogenesis and Triglyceride Synthesis in Nonalcoholic Fatty Liver by Activating SREBP-1c Transcription, Upregulating DGAT1/2 Expression, and Promoting Glycerol Metabolism.","description":"Glycerol kinase (GK) participates in triglyceride (TG) synthesis by catalyzing glycerol metabolism. Whether GK contributes to nonalcoholic fatty liver (NAFL) is unclear. The expression of hepatic Gk is found to be increased in diet-induced and genetic mouse models of NAFL and is positively associated with hepatic SREBP-1c expression and TG levels. Cholesterol and fatty acids stimulate GK expression in hepatocytes. In HFD-induced NAFL mice, knockdown of hepatic Gk decreases expression of SREBP-1c and its target lipogenic genes as well as DGAT1/2, increases serum glycerol levels, decreases serum TG levels, and attenuates hepatic TG accumulation. Overexpression of GK in hepatocytes in mice or in culture produces opposite results. Mechanistic studies reveal that GK stimulates SREBP-1c transcri","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Dec","modification":"2025-04-04T01:20:12.438Z","creation":"2025-04-04T01:20:12.438Z"},"accession":"S-EPMC11633478","cross_references":{"pubmed":["39418169"],"doi":["10.1002/advs.202401311"]}}