{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ghosh S"],"funding":["American Heart Association","NCCIH NIH HHS","NIDDK NIH HHS","National Institute of Diabetes and Digestive and Kidney Diseases","American Heart Association-American Stroke Association","NORC Center Grant","COBRE Center Grant","NIGMS NIH HHS","NIH Common Funds Project","National Medical Research Council, Ministry of Health, Singapore"],"pagination":["17"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4772307"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13"],"pubmed_abstract":["Background
The liver is an important site of fat oxidation, which participates in the metabolic regulation of food intake. We showed previously that mice with genetically inactivated Acads, encoding short-chain acyl-CoA dehydrogenase (SCAD), shift food consumption away from fat and toward carbohydrate when tested in a macronutrient choice paradigm. This phenotypic eating behavior suggests a link between fat oxidation and nutrient choice which may involve an energy sensing mechanism. To identify hepatic processes that could trigger energy-related signals, we have now performed transcriptional, metabolite and physiological analyses in Acads-/- mice following short-term (2 days) exposure to either high- or low-fat diet.Methods and results
Metabolite analysis revealed 25 acylca"],"journal":["Nutrition & metabolism"],"pubmed_title":["Short chain acyl-CoA dehydrogenase deficiency and short-term high-fat diet perturb mitochondrial energy metabolism and transcriptional control of lipid-handling in liver."],"pmcid":["PMC4772307"],"funding_grant_id":["DG-4230068","P20 GM-103528","U24 DK-097153","R21 DK088319","U54 GM104940","R01 DK053113","T32 AT004094","10SDG4230068","R01 DK103860","P20 GM103528","P30 DK072476","R01 DK089641","ID0EF6AE609","53113","U24 DK097153"],"pubmed_authors":["Richards BK","Ghosh S","Kumar KG","Mynatt RL","Simon J","Kruger C","Noland RC","Wicks S","Johnson WD"],"additional_accession":[]},"is_claimable":false,"name":"Short chain acyl-CoA dehydrogenase deficiency and short-term high-fat diet perturb mitochondrial energy metabolism and transcriptional control of lipid-handling in liver.","description":"Background
The liver is an important site of fat oxidation, which participates in the metabolic regulation of food intake. We showed previously that mice with genetically inactivated Acads, encoding short-chain acyl-CoA dehydrogenase (SCAD), shift food consumption away from fat and toward carbohydrate when tested in a macronutrient choice paradigm. This phenotypic eating behavior suggests a link between fat oxidation and nutrient choice which may involve an energy sensing mechanism. To identify hepatic processes that could trigger energy-related signals, we have now performed transcriptional, metabolite and physiological analyses in Acads-/- mice following short-term (2 days) exposure to either high- or low-fat diet.Methods and results
Metabolite analysis revealed 25 acylca","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016","modification":"2026-06-12T05:40:15.102Z","creation":"2019-03-26T22:34:20Z"},"accession":"S-EPMC4772307","cross_references":{"pubmed":["26933443"],"doi":["10.1186/s12986-016-0075-0"]}}