biostudies-literatureGhosh SAmerican Heart AssociationNCCIH NIH HHSNIDDK NIH HHSNational Institute of Diabetes and Digestive and Kidney DiseasesAmerican Heart Association-American Stroke AssociationNORC Center GrantCOBRE Center GrantNIGMS NIH HHSNIH Common Funds ProjectNational Medical Research Council, Ministry of Health, Singapore17https://www.ebi.ac.uk/biostudies/studies/S-EPMC4772307biostudies-literatureUnknown13<h4>Background</h4>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.<h4>Methods and results</h4>Metabolite analysis revealed 25 acylcaNutrition & metabolismShort chain acyl-CoA dehydrogenase deficiency and short-term high-fat diet perturb mitochondrial energy metabolism and transcriptional control of lipid-handling in liver.PMC4772307DG-4230068P20 GM-103528U24 DK-097153R21 DK088319U54 GM104940R01 DK053113T32 AT00409410SDG4230068R01 DK103860P20 GM103528P30 DK072476R01 DK089641ID0EF6AE60953113U24 DK097153Richards BKGhosh SKumar KGMynatt RLSimon JKruger CNoland RCWicks SJohnson WDfalseShort chain acyl-CoA dehydrogenase deficiency and short-term high-fat diet perturb mitochondrial energy metabolism and transcriptional control of lipid-handling in liver.<h4>Background</h4>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.<h4>Methods and results</h4>Metabolite analysis revealed 25 acylca2016-01-01T00:00:00Z20162026-06-12T05:40:15.102Z2019-03-26T22:34:20ZS-EPMC47723072693344310.1186/s12986-016-0075-0