%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/