CPT1A and metabolic syndrome: Collectively, these data suggest that: (1) under normal, healthy conditions the potential to increase β-oxidation may be primarily via CPT1-mediated mechanisms, (2) MetS may be associated with impaired CPT1A-mediated β-oxidation, which is supported by the lack of CPT1A abundance increase during the glucose challenge in the OLETF, ARB and MINUS groups, and (3) that non-compliance (MINUS) may be associated with impaired β-oxidation via CPT1A to a greater extent than untreated (OLETF) conditions.