RNA-Seq of liver from CLA-exposed mice with/without PPARα antagonist

We demonstrate that conjugated linoleic acid (CLA), when given to mice as a dietary supplement, induced an enlarged liver and hepatic steatosis. The progression of NAFLD and insulin resistance was reversed by GW6471 a small-molecule antagonist of PPARα. Transcriptional profiling of livers unraveled that genes involved in lipid metabolism core gene programs controlled by PPARα in response to CLA and GW6471.Our findings reveal a novel role of PPARα in the regulation of lipid homeostasis and highlight its druggable nature in NAFLD. Hepatic mRNA profiles of mice treated with CLA or PPARα antagonist or CLA combined PPARα antagonist