{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Helsley RN"],"funding":["National Center for Advancing Translational Sciences","National Center for Research Resources","Alnylam Pharmaceuticals","NICHD NIH HHS","NCATS NIH HHS","NIDDK NIH HHS","NASPGHAN Foundation","NCI NIH HHS","National Institutes of Health","NIGMS NIH HHS","NIH HHS"],"pagination":["25-42"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10679901"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["79(1)"],"pubmed_abstract":["Background & aims
The consumption of sugar and a high-fat diet (HFD) promotes the development of obesity and metabolic dysfunction. Despite their well-known synergy, the mechanisms by which sugar worsens the outcomes associated with a HFD are largely elusive.Methods
Six-week-old, male, C57Bl/6 J mice were fed either chow or a HFD and were provided with regular, fructose- or glucose-sweetened water. Moreover, cultured AML12 hepatocytes were engineered to overexpress ketohexokinase-C (KHK-C) using a lentivirus vector, while CRISPR-Cas9 was used to knockdown CPT1α. The cell culture experiments were complemented with in vivo studies using mice with hepatic overexpression of KHK-C and in mice with liver-specific CPT1α knockout. We used comprehensive metabolomics, electron micros"],"journal":["Journal of hepatology"],"pubmed_title":["Ketohexokinase-C regulates global protein acetylation to decrease carnitine palmitoyltransferase 1a-mediated fatty acid oxidation."],"pmcid":["PMC10679901"],"funding_grant_id":["K01 DK128022","R01 DK121967","UL1TR001998","K12 HD000850","P30 GM127211","K01DK128022","P30 DK036836","T32 CA165990","UL1 TR001998","S10 OD028654","1S10 OD028654"],"pubmed_authors":["Sun RC","Softic S","Meyer JG","Helsley RN","Rose J","Schilling B","Bons J","Romero MDM","Kahn CR","King CD","Herrero L","Conroy LR","Park SH","Sullivan PG","Vekaria HJ"],"additional_accession":[]},"is_claimable":false,"name":"Ketohexokinase-C regulates global protein acetylation to decrease carnitine palmitoyltransferase 1a-mediated fatty acid oxidation.","description":"Background & aims
The consumption of sugar and a high-fat diet (HFD) promotes the development of obesity and metabolic dysfunction. Despite their well-known synergy, the mechanisms by which sugar worsens the outcomes associated with a HFD are largely elusive.Methods
Six-week-old, male, C57Bl/6 J mice were fed either chow or a HFD and were provided with regular, fructose- or glucose-sweetened water. Moreover, cultured AML12 hepatocytes were engineered to overexpress ketohexokinase-C (KHK-C) using a lentivirus vector, while CRISPR-Cas9 was used to knockdown CPT1α. The cell culture experiments were complemented with in vivo studies using mice with hepatic overexpression of KHK-C and in mice with liver-specific CPT1α knockout. We used comprehensive metabolomics, electron micros","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jul","modification":"2025-04-22T18:09:17.742Z","creation":"2025-04-06T02:21:43.819Z"},"accession":"S-EPMC10679901","cross_references":{"pubmed":["36822479"],"doi":["10.1016/j.jhep.2023.02.010"]}}