Fatty acids are activated for degradation by conjugation with coenzyme A CoA in the cytosol. The long-chain fatty-acyl-CoA is then modified by carnitine palmitoyltransferase 1 CPT1 to acylcarnitine and transported across the inner mitochondrial membrane by carnitine translocase CAT.
CPT2 then coverts the long chain acylcarnitine back to long-chain acyl-CoA before beta-oxidation. Schematic diagram of fatty acid transport and beta-oxidation in the mitochondria. Adipose tissue and lactating mammary glands also take up glucose from the blood for conversion into triglycerides.
Effect of Pyruvate and Acetoacetate on the Metabolism of Fatty Acids by the Perfused Rat Heart
This occurs in the same way as it does in the liver, except that these tissues do not release the triglycerides thus produced as VLDL into the blood. All cells in the body need to manufacture and maintain their membranes and the membranes of their organelles. Whether they rely for this entirely on free fatty acids absorbed from the blood, or are able to synthesize their own fatty acids from the blood glucose, is not known. The cells of the central nervous system will almost certainly have the capability of manufacturing their own fatty acids, as these molecules cannot reach them through the blood brain barrier , while, on the other hand, no cell in the body can manufacture the required essential fatty acids which have to be obtained from the diet and delivered to each cell via the blood.
Much like beta-oxidation , straight-chain fatty acid synthesis occurs via the six recurring reactions shown below, until the carbon palmitic acid is produced. The diagrams presented show how fatty acids are synthesized in microorganisms and list the enzymes found in Escherichia coli. FASII is present in prokaryotes , plants, fungi, and parasites, as well as in mitochondria.
In animals, as well as some fungi such as yeast, these same reactions occur on fatty acid synthase I FASI , a large dimeric protein that has all of the enzymatic activities required to create a fatty acid.
Dynamic Adaptation of Nutrient Utilization in Humans
FASI is less efficient than FASII; however, it allows for the formation of more molecules, including "medium-chain" fatty acids via early chain termination. They also have the job of synthesizing bioactive lipids as well as their precursor molecules. Elongation, starting with stearate , is performed mainly in the endoplasmic reticulum by several membrane-bound enzymes. The enzymatic steps involved in the elongation process are principally the same as those carried out by fatty acid synthesis , but the four principal successive steps of the elongation are performed by individual proteins, which may be physically associated.
NADPH is also formed by the pentose phosphate pathway which converts glucose into ribose, which can be used in synthesis of nucleotides and nucleic acids , or it can be catabolized to pyruvate. In humans, fatty acids are formed from carbohydrates predominantly in the liver and adipose tissue , as well as in the mammary glands during lactation. The cells of the central nervous system probably also make most of the fatty acids needed for the phospholipids of their extensive membranes from glucose, as blood-born fatty acids cannot cross the blood brain barrier to reach these cells.
The pyruvate produced by glycolysis is an important intermediary in the conversion of carbohydrates into fatty acids and cholesterol. However, this acetyl CoA needs to be transported into cytosol where the synthesis of fatty acids and cholesterol occurs.
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This cannot occur directly. To obtain cytosolic acetyl-CoA, citrate produced by the condensation of acetyl CoA with oxaloacetate is removed from the citric acid cycle and carried across the inner mitochondrial membrane into the cytosol. The oxaloacetate is returned to mitochondrion as malate and then converted back into oxaloacetate to transfer more acetyl-CoA out of the mitochondrion. Acetyl-CoA is formed into malonyl-CoA by acetyl-CoA carboxylase , at which point malonyl-CoA is destined to feed into the fatty acid synthesis pathway.
See how fatty acids are broken down and used to generate ATP.
Acetyl-CoA carboxylase is the point of regulation in saturated straight-chain fatty acid synthesis, and is subject to both phosphorylation and allosteric regulation. Regulation by phosphorylation occurs mostly in mammals, while allosteric regulation occurs in most organisms. Allosteric control occurs as feedback inhibition by palmitoyl-CoA and activation by citrate. When there are high levels of palmitoyl-CoA, the final product of saturated fatty acid synthesis, it allosterically inactivates acetyl-CoA carboxylase to prevent a build-up of fatty acids in cells.
Citrate acts to activate acetyl-CoA carboxylase under high levels, because high levels indicate that there is enough acetyl-CoA to feed into the Krebs cycle and produce energy.
High plasma levels of insulin in the blood plasma e. Disorders of fatty acid metabolism can be described in terms of, for example, hypertriglyceridemia too high level of triglycerides , or other types of hyperlipidemia. These may be familial or acquired. Familial types of disorders of fatty acid metabolism are generally classified as inborn errors of lipid metabolism. These disorders may be described as fatty oxidation disorders or as a lipid storage disorders , and are any one of several inborn errors of metabolism that result from enzyme defects affecting the ability of the body to oxidize fatty acids in order to produce energy within muscles, liver, and other cell types.
From Wikipedia, the free encyclopedia. Main article: Fatty acid synthesis. In: Biochemistry Fourth ed. New York: W. Freeman and Company. Molecular Aspects of Medicine. Jul J Neurosci. Feb J Cereb Blood Flow Metab.
Fatty acid synthesis - Wikipedia
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