In humans, it has been described that during physiological hyperglycemia with hyperinsulinemia and maintained FFA concentrations (i.e., a condition that mimics the insulin-resistant state), human skeletal muscle malonyl-CoA concentrations are significantly increased and are directly associated with a reduction in LCFA oxidation and functional CPT-1 activity [27]. The gene discussed is CPT1A; the disease is Hyperinsulinemia.