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Folate metabolism, diagram

A more complete versit>n of folate metabolism is given in Figure 9.5, The cycle of reactions used to regenerate methionine is featured In the center of the diagram. H4folate may be considered the starting and ending point in the cycles depicted. The cycles involve the introduction of a I-carbon unit, derived from serine, into tissue folates. This is followed by use of the 1-carbon unit for the synthesis of methionine, purines, and thymidylate. Conditions that result in a decline in tissue... [Pg.497]

Fic. 3. Abbreviated diagram of folate metabolism. DHF, dihydrofolate THF, tetrahydro-... [Pg.237]

FIG. 2. Schematic diagram of whole-body folate metabolism. Dietary forms of polyglutamyl folates are deconjugated in the jejunum (vertical rectangle on left) by mucosal and, to a lesser extent, pancreatic hydrolases. Secretion of folate in bite accounts for an enterohepatic circulation that has not been incorporated into modeling. Tissues behave, at least superficially, as a large, kinetically slow, pool. [Pg.84]

Figure 22.6 How various factors increase the risk of atherosclerosis, thrombosis and myocardial infarction. The diagram provides suggestions as to how various factors increase the risk of development of the trio of cardiovascular problems. The factors include an excessive intake of total fat, which increases activity of clotting factors, especially factor VIII an excessive intake of saturated or trans fatty acids that change the structure of the plasma membrane of cells, such as endothelial cells, which increases the risk of platelet aggregation or susceptibility of the membrane to injury excessive intake of salt - which increases blood pressure, as does smoking and low physical activity a high intake of fat or cholesterol or a low intake of antioxidants, vitamin 6 2 and folic acid, which can lead either to direct chemical damage (e.g. oxidation) to the structure of LDL or an increase in the serum level of LDL, which also increases the risk of chemical damage to LDL. A low intake of folate and vitamin B12 also decreases metabolism of homocysteine, so that the plasma concentration increases, which can damage the endothelial membrane due to formation of thiolactone. Figure 22.6 How various factors increase the risk of atherosclerosis, thrombosis and myocardial infarction. The diagram provides suggestions as to how various factors increase the risk of development of the trio of cardiovascular problems. The factors include an excessive intake of total fat, which increases activity of clotting factors, especially factor VIII an excessive intake of saturated or trans fatty acids that change the structure of the plasma membrane of cells, such as endothelial cells, which increases the risk of platelet aggregation or susceptibility of the membrane to injury excessive intake of salt - which increases blood pressure, as does smoking and low physical activity a high intake of fat or cholesterol or a low intake of antioxidants, vitamin 6 2 and folic acid, which can lead either to direct chemical damage (e.g. oxidation) to the structure of LDL or an increase in the serum level of LDL, which also increases the risk of chemical damage to LDL. A low intake of folate and vitamin B12 also decreases metabolism of homocysteine, so that the plasma concentration increases, which can damage the endothelial membrane due to formation of thiolactone.

See other pages where Folate metabolism, diagram is mentioned: [Pg.499]    [Pg.499]    [Pg.496]    [Pg.496]   
See also in sourсe #XX -- [ Pg.237 ]




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