In the present study, chronic HFD feeding suppressed PPARα activation in the liver, which, in turn, downregulated lipolysis and fatty acid oxidation-related gene levels (LPL, CPT-1a, and ACOX1) (Figure 6 and Figure 7) and ultimately led to hepatic lipid deposition and dyslipidemia (Figure 4 and Figure 5). The gene discussed is CPT1A; the disease is metabolic syndrome.