Fatty acids, oxidation mobilization

Mobilization of Fats from Dietary Intake and Adipo.se Ti.ssne /3-Oxidation of Fatty Acids /3-Oxidation of Odd-Carbon Fatty Acids /3-Oxidation of Unsatnrated Fatty Acids Other Aspects of Fatty Acid Oxidation... 

A. Mobilization of fat stores allows fats to be burned to produce energy via fatty acid oxidation. 

Hormone-sensitive lipase PMRRSV Triacylglycerol mobilization and fatty acid oxidation... 

New section on the role of perilipin phosphorylation in the control of fat mobilization New discussion of the role of acetyl-CoA in the integration of fatty acid oxidation and synthesis... 

Excess acetate (C2) can be converted to the mobile ketone body energy source aceto-acetate (C4) and thence its reduced form hydroxybutyrate (C,) for transport throughout the body. Excess acetate can be carboxylated (via acetylCoA carboxylase) to form malonylCoA (C3), the donor for further C2 additions (with C02 elimination) in the anabolic synthesis of long chain fatty acids. Fatty acids are components of the phospholipids of cellular membranes and are also stored as triacylglycerols (triglycerides) for subsequent hydrolysis and catabolic fatty acid oxidation to yield reduced coenzymes and thence ATP (see Chapter 2). 

The ability to maintain glucose homeostasis during the first few days of life also depends on the activation of gluconeogenesis and the mobilization of fatty acids. Fatty acid oxidation in the liver not only promotes gluconeogenesis (see Chapter 31) but generates ketone bodies. The neonatal brain has an enhanced capacity to use ketone bodies relative to that of infants (fourfold) and adults (40-fold). This ability is consistent with the relatively high fat content of breast milk. 

As the intensity of exercise increases further, such as occurs in a competitive marathon race, both fatty acid oxidation and glucose oxidation determine the rate of ATP supply. Muscle glycogen is mobilized, and its concentration steadily decreases at a rate that is proportional to the intensity of the exercise. 

EXAMPLE 13.27 If muscle uses fatty acid oxidation to supply ATP, then less glycogen is mobilized so any exercise/diet strategies that increase the proportion of energy derived from fatty acids should save glycogen. Training increases the activity of the P-oxidation enzymes (Sec. 10.5), and a good supply of carnitine should also assist in fatty acid catabolism. 

The lipid stores are also mobilized after birth. Within minutes the blood levels of free fatty acid increase markedly as a result of lipolysis. The fatty acid oxidation yields acetyl CoA which is converted to ketone bodies which can readily be used as a source of energy by the brain. Of course with normal feeding the muscle and liver stores are soon restored. 

If the direct feedback link is strong, so that the flux is very sensitive to regulators of the tricarboxylic acid cycle, the flux will not be sensitive to changes in extracellular fatty acid concentration, resulting from increased mobilization from the adipose tissue reserves. This would be unfortunate since the extracellular fatty acid concentration is an important signal for tissues to increase their rate of fatty acid oxidation when carbohydrate stores are being depleted (carbohydrate stress). However, if a branch point exists at the level of acetyl-CoA, the resulting branched system provides feedback indirectly, as discussed in Section II. [Such a branch could be the pathway that produces ketone bodies (in the liver) or deacylation to acetate which may occur in some tissues—see Knowles et al. (28) and Buckley and Williamson (6). ... 

Alcoholism leads to fat accumulation in the liver, hyperlipidemia, and ultimately cirrhosis. The exact mechanism of action of ethanol in the long term is stiU uncertain. Ethanol consumption over a long period leads to the accumulation of fatty acids in the liver that are derived from endogenous synthesis rather than from increased mobilization from adipose tissue. There is no impairment of hepatic synthesis of protein after ethanol ingestion. Oxidation of ethanol by alcohol dehydrogenase leads to excess production of NADH. 

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