Most of the proteins and other molecules that make up mitochondria originate in the cell nucleus. However, 37 genes are contained in the human mitochondrial genome, 13 of which produce various components of the electron transport chain (ETC). In many organisms, the mitochondrial genome is inherited maternally. This is because the mother’s egg cell donates the majority of cytoplasm to the embryo, and mitochondria inherited from the father’s sperm are usually destroyed.
Mitochondrial fatty acid β-oxidation (FAO) is the most efficient and predominant substrate for energy production in the normal adult human heart, with glucose oxidation, glycolysis, lactate, and ketones additionally contributing to myocardial ATP production.1
The relative contribution of fatty acids diminishes with enhanced reliance on glucose utilization during the development of cardiac hypertrophy.
Whole-body insulin resistance can affect cardiac energy metabolism, even in structurally normal hearts. Patients with type 2 diabetes mellitus who have otherwise normal cardiac function regenerate phosphocreatine at a significantly lower rate after exercise than control subjects without diabetes mellitus.32 In patients with cardiomyopathy, the development of insulin resistance is linked to increased sympathetic signaling, which leads to liberation of free fatty acids from adipose tissue into the bloodstream.33 Thus, in the failing myocardium, decreases in insulin sensitivity can lead to further reductions in glucose oxidation and deteriorations in cardiac function by depriving the heart of access to a more metabolically efficient substrate.
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