The major sites of regulation of fatty acid entry into myocellular mitochondria. Insulin inhibits (–) lipolysis, thus lowering FFA concentrations and limiting FFA availability for transport into muscle. Insulin stimulates (+) muscle glucose uptake, oxidation, and storage. Malonyl-CoA, generated as a result of insulin-stimulated glucose metabolism, inhibits CPT-1 and further reduces LCFA entry into the mitochondria. CPT-1 is not needed for MCFA to enter the mitochondria. The processes that regulate intramyocellular triglyceride synthesis and breakdown in humans are largely unknown.