Fats are normally the major source of energy in liver and in muscle, and in human tissues in general, except for red cells and brain. Triglycerides are the storage and transport form of fats; fatty acids are the immediate source of energy. They are released from adipose tissue, transported in association with plasma albumin, and delivered to cells for metabolism. The catabolism of fatty acids is entirely oxidative; after they have been transported through the cytoplasm, their oxidation proceeds in both the peroxisome and the mitochondrion, primarily by a cycle of reactions known as β-oxidation. Carbons are released, two at a time, from the carboxyl end of the fatty acid; the major end-products are acetyl-coenzyme A (acetyl-CoA) and the reduced forms of the nucleotides, flavin adenine dinucleotide and nicotinamide adenine dinucleotide (FADH2 and NADH, respectively). In muscle, the acetyl-CoA is metabolized via the tricarboxylic acid (TCA) cycle and oxidative phosphorylation to produce ATP; in liver, it is shunted largely to the synthesis of ketone bodies (ketogenesis), which are water-soluble lipid derivatives that, like glucose , are exported from liver for use in other tissues. Fat metabolism is controlled primarily by the rate of triglyceride hydrolysis (lipolysis) in adipose tissue, regulated by hormonal mechanisms involving insulin and glucagon, epinephrine, and cortisol. These hormones coordinate the metabolism of carbohydrate, lipid and protein throughout the body (see Chapter 20).
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