of cardiac ATP production ( 1 ). FAs are also incorporated into triacylglycerol (TG), which is stored in lipid droplets. Cardiac TG turnover is rapid ( 2 ) and FAs released from TG can contribute up to 10-20% of ATP production ( 3 ). Plasma FA and TG levels rise in insulin resistance and diabetes ( 4, 5 ), and cardiac FA utilization can increase to supply as much as 90% of ATP ( 6, 7 ). Despite this increase in FAO, FA uptake can exceed the ability of the heart to utilize FAs, leading to excess accumulation of TG in cardiomyocytes ( 6-9 ). The compensatory changes that occur in response to excessive FA availability eventually become maladaptive, and the heart is locked in a pathological and infl exible metabolic state that contributes to cardiac dysfunction ( 6, 7, 10 ). As such, maintenance of metabolic fl exibility is essential for normal cardiac function. Whereas many proteins have been identifi ed to contribute to cardiac FA uptake and metabolism ( 1, 10 ), relatively little information is available about the role of lipin-1 in the heart. Lipin-1 is an important protein involved in regulating both TG synthesis and FAO in other organs ( 11 ).Instead of being considered as mutually antagonistic processes, FAO and TG synthesis are now widely viewed as being companion pathways because augmenting cardiac TG synthesis increases FAO ( 12 ). Moreover, FAs released through lipolysis of endogenous TG stores contribute signifi cantly to FAO ( 3,13 ). Lipin-1 could play a prominent role in this regulation as it is a bifunctional protein involved in regulating both TG synthesis and FAO in the The constant requirement for ATP in the beating heart is satisfi ed by the utilization of diverse substrates, such as fatty acids (FA), glucose, lactate, ketones, and amino acids, with FA oxidation (FAO) providing the majority (50-75%)