Abstract
This chapter presents the molecular, genetic, and cellular basis of fatty acid, lipid, and glucose metabolic defects that can lead to cardiac disease. Fatty acids and lipids play an integral role in cardiomyocyte structure and function. In the postnatal and adult mammalian heart, fatty acid β-oxidation is the preferred pathway for the energy required for normal cardiac function. Glucose metabolism, which provides the bulk of ATP during prenatal growth, contributes significantly to the ATP production in the adult heart. In myocardial ischemia and hypertrophy, profound changes in both glucose and fatty acid metabolism occur, with glucose metabolism taking on greater importance. Additionally, specific abnormalities in myocardial fatty acid oxidation (FAO) metabolism, caused by either inherited or acquired physiological stresses; and in cardiac glucose use, caused by chronic insulin deficiency or resistance, may result in dysrhythmias, cardiomyopathy, and heart failure (HF). Abnormalities in glucose and fatty acid metabolism associated with diabetes and metabolic syndrome (MetSyn), and chronic diseases that are becoming increasingly prevalent in the urbanized world, also have associated cardiovascular abnormalities, ranging from hypertension to increased cardiomyopathy and HF.
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