CPT1B and diabetes mellitus: Considered together with the increase in total fatty acid oxidation activity and mRNA levels of the mCPT-1 gene, which encodes the rate-limiting enzyme in mitochondrial β-oxidation, it suggests that the type 2 diabetic heart removed more fatty acids from circulation to provide energy though mitochondrial β-oxidation; this supports the common view that in diabetes, the FA supply is in excesses, causing the increased cellular oxidative capacity, intracellular TG and FFA accumulation, which is associated with lipotoxicity[25].