Impaired trafficking of fatty acids between oxidative disposal in nonadipose tissues and storage in adipose tissue, leading to ectopic lipid accumulation, may be causative in impaired glucose control [1], dyslipidemia [2], and inflammation [3], all important factors in the etiology of type 2 diabetes and cardiovascular disease. Metabolic flexibility is defined as the ability to switch from predominantly lipid metabolism, with high fluxes of fatty acids in the fasting state, to enhanced glucose uptake, oxidation and storage under hyperinsulinemic conditions [4]. Impaired metabolic flexibility could in theory induce ectopic lipid accumulation either via defective control of fatty acid availability due to insulin resistance [5, 6] or impaired fatty acid oxidation capacity [7, 8] or both.
