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Hydrolysis occurs via the action of the adipose tissue enzyme hormone-sensitive lipase. The activity of this lipase is suppressed by insulin. When plasma insulin concentrations fall in the postabsorptive state, hormone-sensitive lipase is activated to release more free fatty streak fatty acids into the circulation. Thus, in the postabsorptive state, free fatty acid concentrations in plasma are high; conversely, fatty streak in the postprandial state, hormone-sensitive lipase activity is suppressed and free fatty acid concentrations in plasma are low. Free fatty acids circulate in the blood bound to albumin. The major site of fatty acid oxidation is skeletal muscle. When free fatty acid fatty streak concentrations are relatively high, muscle uptake of fatty acids is also high. As in liver, fatty acids in the muscle are transported via a carnitine-dependent pathway into mitochondria where they undergo β-oxidation, which involves removal of two carbon fragments. These two carbon units enter the citric acid cycle as acetyl coenzyme A (CoA), through which they are completely oxidized to carbon dioxide with the generation of large quantities of high-energy phosphate bonds, or they condense to form ketone bodies.
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