March 2001
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Fatty acids provide highly efficient energy storage, storing much more energy for their weight than carbohydrates like glucose. Fatty acids are stored as triglycerides in adipose tissue, in which each triglyceride molecule contains three fatty acids and one glycerol. Triglycerides form fatty droplets that exclude water and take up minimal space. Fatty acids are also more highly reduced than carbohydrates, so they provide more energy during oxidation. The efficiency of energy storage in fats is probably an important reason why animals store most of their energy as fats and only a small amount of energy as carbohydrates.
When glucose levels are low during long periods between meals the enzyme glucagon secreted by the pancreas stimulates adipose lipase activity to release fatty acids from triglycerides. Epinephrine can stimulate the same activity to release energy during the fight or flight response. Once released, these fatty acids travel through the blood to other tissues such as muscle where they are oxidized to provide energy through the mitochondrial beta-oxidation pathway. Since fatty acid beta-oxidation occurs in the mitochondrial matrix, long-chain fatty acids must be actively transported from the cytoplasm into mitochondria by carnitine palmitoyl transferase (see Pathway).
The chemical energy contained in fatty acids is released through the beta-oxidation of fatty acids in mitochondria. The beta-oxidation pathway includes four reactions that occur in repeating cycles with each fatty acid molecule. In each cycle, a fatty acid is progressively shortened by two carbons as it is oxidized and its energy captured by the reduced energy carriers NADH and FADH2. At the end of each cycle of four reactions, one acetyl-CoA two-carbon unit is released from the end of the fatty acid, which then goes through another round of beta-oxidation, continuing to oxidize and shorten even-chain fatty acids until they are entirely converted to acetyl-CoA. Fatty acids with an odd number of carbons in the acyl chain are left at the end with propionyl-CoA, with 3 carbons, which cannot enter another round of beta-oxidation. The propionyl-CoA produced in this manner is converted to succinyl-CoA that then enters the Krebs cycle (see pathway).
The acetyl-CoA generated in beta-oxidation enters the Krebs cycle, where it is further oxidized to CO2, producing more reduced energy carriers, NADH and FADH2 (See Krebs cycle pathway). These carriers produced in the Krebs cycle, along with those produced directly in beta-oxidation, transfer their energy to the electron transport chain where they drive the creation of the proton gradient that supports mitochondrial ATP production. Another destination of acetyl-CoA is the production of ketone bodies by the liver that are transported to tissues like the heart and brain for energy (See pathway).
Defects in fat metabolism associated with clinical disorders include lack of carnitine or carnitine transferase, which can lead to weakness and muscle pain during exercise. Defects in acyl-CoA dehydrogenase, which catalyzes the first step in beta-oxidation, appear to be involved in some cases of sudden infant death syndrome. |
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Glenn Croston, PhD |
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