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Libros sobre el tema "Folic acid Metabolism"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 9 de junio de 2025

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1

Frances, Picciano Mary, Stokstad E. L. Robert, Gregory Jesse F, and American Chemical Society. Food and Nutritional Biochemistry Subdivision., eds. Folic acid metabolism in health and disease. New York: Wiley-Liss, 1990.

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2

Bailey, Lynn B. Folate in health and disease. 2nd ed. Boca Raton: Taylor & Francis, 2010.

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3

J, Massaro Edward, and Rogers John M, eds. Folate and human development. Totowa, N.J: Humana Press, 2002.

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4

Amouzou, Kou'santa Sabiba. Evaluation des marqueurs nutritionnels et génétiques du statut en coenzymes B (cobalamines et folates) et de l'homocystéinemie plasmatique dans une population d'Afrique de l'Ouest (Benin-Togo). Lomé: [s.n., 2003.

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5

Pristoupilova, Kamila. Role of folates in metabolic pathways (Studie AV CR). Academia, 1997.

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6

Folate in health and disease. 2nd ed. Boca Raton: Taylor & Francis, 2010.

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7

Hitchings, George H. Inhibition of Folate Metabolism in Chemotherapy: The Origins and Uses of Co-trimoxazole. Brand: Springer, 2011.

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8

Folate in Health and Disease. 2nd ed. CRC, 2009.

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9

Bailey, Lynn B. Folate in Health and Disease. Taylor & Francis Group, 1994.

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10

Bailey, Lynn B. Folate in Health and Disease. Taylor & Francis Group, 2009.

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11

Bailey, Lynn B. Folate in Health and Disease. Taylor & Francis Group, 2009.

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12

Bailey, Lynn B. Folate in Health and Disease. Taylor & Francis Group, 2009.

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13

Bailey, Lynn B. Folate in Health and Disease. Taylor & Francis Group, 2009.

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14

Bailey, Lynn B. Folate in Health and Disease. Taylor & Francis Group, 1994.

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15

Rogers, John M., and Edward J. Massaro. Folate and Human Development. Humana Press, 2010.

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16

Rogers, John M., and Edward J. Massaro. Folate and Human Development. Humana Press, 2002.

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17

Rogers, John M., and Edward J. Massaro. Folate and Human Development. Humana Press, 2013.

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18

Acar, J. F., and G. H. Hitchings. Inhibition of Folate Metabolism in Chemotherapy: The Origins and Uses of Co-Trimoxazole. Springer London, Limited, 2012.

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19

Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Vitamin B9 (folate) in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0012.

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Folate is a coenzyme in multiple biochemical pathways involving one-carbon metabolism, including amino acid metabolism, DNA and RNA synthesis, homocysteine metabolism, and methylation of DNA. The most overt consequence of folate deficiency is megaloblastic anaemia caused by the inhibition of DNA synthesis in red blood cell production. Folate deficiency may also influence the ability to maintain DNA methylation patterns in replicating cells, resulting in lasting phenotypic changes. Embryogenesis and fetal growth require higher levels of folate, which must be supplied maternally during pregnancy. A link between low maternal folate levels and the occurrence of neural tube defects has long been recognized. Other effects in pregnancy include increased risks of pre-eclampsia and placental vascular disorders. The general recommendation is for supplementation prior to conception and throughout pregnancy with 400 #amp;#x03BC;g of folic acid in tablet form, in addition to dietary sources, which can reduce the risk of neural tube defects.
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20

Silva, Aminda De, J. A. Saunders, and M. A. Stroud. Vitamin deficiencies. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0333.

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Vitamins are organic compounds required by the body in small amounts to perform specific cellular functions. Nine vitamins (thiamine (vitamin B1), riboflavin (vitamin B2), pyridoxine (vitamin B6), cyanocobalamin (vitamin B12), niacin (nicotinic acid; vitamin B3), pantothenic acid (vitamin B5), biotin (vitamin B7; vitamin H), folic acid (folate; vitamin B9), and ascorbic acid (vitamin C)) are water soluble, while four (vitamins A, D, E, and K) are fat soluble. The importance of vitamins was first appreciated through recognition of their clinical deficiency state. However, this approach has led to the concept that the primary purpose of a vitamin is to prevent the associated clinical deficiency state and, consequently, unless patients exhibit signs of a specific clinical deficiency state, they are thought to be replete in the corresponding vitamin. This is a misunderstanding. In reality, most vitamins have many different functions which are incompletely understood, and impaired biochemical function and even functional problems affecting metabolic, immunological, or cognitive status can occur with marginal vitamin depletion long before overt clinical deficiency becomes evident. A high index of suspicion is thus essential in all patients who have malnutrition or malabsorption, to ensure that levels that might compromise health, resistance to disease, and recovery from injury or illness are not left untreated.
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