%0 Journal Article %T Short chain acyl-CoA dehydrogenase deficiency and short-term high-fat diet perturb mitochondrial energy metabolism and transcriptional control of lipid-handling in liver %A Brenda K. Richards %A Claudia Kruger %A Jacob Simon %A K. Ganesh Kumar %A Randall L. Mynatt %A Robert C. Noland %A Shawna Wicks %A Sujoy Ghosh %A William D. Johnson %J Archive of "Nutrition & Metabolism". %D 2016 %R 10.1186/s12986-016-0075-0 %X 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 %K Short chain acyl-CoA dehydrogenase deficiency %K Fatty acid beta-oxidation %K Mitochondrial %U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4772307/