Urinary excretion of 5-methyltetrahydrofolate and liver S-adenosylmethionine levels of rats fed a vitamin B1 2-deficient diet

Vidal, A.J.; Stokstad, E. L. R.

doi:10.1016/0304-4165(74)90217-7

Cited by 35 publications

(8 citation statements)

References 21 publications

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“…In spite of these regulatory mechanisms the liver concentration of S-adenosylmethionine is decreased in vitamin B,,-deficient rats (Vidal & Stokstad, 1974) and sheep (Gawthorne & Smith, 1974). The levels are normalized after the administration of methionine.…”

Section: Discussionmentioning

confidence: 96%

Effect of Vitamin B₁₂deficiency on phosphatidylethanolamine methylation in rat liver

Åkesson¹,

Fehling²,

Jägerstad³

1978

Br J Nutr

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I. In vitamin B12 deficiency the activity of tetrahydropteroylglutamate methyltransferase (EC 2 . I . I .13) is depressed and the synthesis of methionine is reduced. Because the methyl group of methionine is largely utilized for the methylation of phosphatidylethanolamine, we investigated the effects of vitamin Bla deficiency on phosphatidylcholine synthesis. Chemical analysis of liver phospholipids showed that the vitamin Bl,-deficient rats had a higher proportion of phosphatidylethanolamine and a lower proportion of phosphatidylcholine, indicating that the impaired synthesis of phosphatidylcholine by methylation leads to changes in membrane phospholipid composition.

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Section: Discussionmentioning

confidence: 96%

Effect of Vitamin B₁₂deficiency on phosphatidylethanolamine methylation in rat liver

Åkesson¹,

Fehling²,

Jägerstad³

1978

Br J Nutr

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“…It also acts in many trans-sulphuration reactions. 122 Clinical studies initially demonstrated a de®nite bene®t of treatment with SAMe on both the symptomatology and biochemistry in OC 123±125 This was later con®rmed in a single blind, placebocontrolled trial in which six patients received high dose (800mg/day) intravenous SAMe. 120 As an increase in the metabolically inert biliary methylated derivatives of oestrogen was found the effect was attributed to decreased oestrogen bioavailability.…”

Section: S-adenosyl-l-methioninementioning

confidence: 99%

Obstetric cholestasis

Raine‐Fenning

Kilby

1997

Fet. Matern. Med. Rev.

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“…It is, therefore, possible that intracellular metabolism is not significantly changed and SAMe may selectively alter plasma membrane phosphatidylcholine content and fluidity. On the other hand, SAMe may just serve as a source for peripheral production of methionine which is rapidly transported into hepatocytes where it is a major determinant of intracellular SAMe concentrations (134).…”

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confidence: 99%

Estrogen-Induced Cholestasis: Clues to Pathogenesis and Treatment

1983

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EditorialsEstrogen-Induced Cholestasis: Clues to Pathogenesis and Treatment Estrogen-related cholestasis has been of clinical interest for nearly three decades. The clinical spectrum of intrahepatic cholestasis of pregnancy and pruritus gravidarum was first characterized in 1955 (1-5). Although its pathogenesis remains unknown, epidemiologic and experimental data suggest an inheritable abnormality in hepatic reactivity to circulating estrogens. Oral contraceptives were introduced in 1960. It was soon observed that a small percentage of women using these drugs develop intrahepatic cholestasis (6-10, Sotaniemi, E. et al. Brit Med J 1964; 2:1264-1265, Correspondence) and approximately 50% of these individuals have intrahepatic cholestasis of pregnancy (11-13, Holzbach, R. T. and Sanders, H. H. Gastroenterology 1965;482322, Abstract). A "cholestatic" response to oral contraceptive steroids was noted in several hepatic disorders, including cirrhosis and the Dubin-Johnson syndrome (14-16). Data from rechallenge experiments suggests that the estrogenic component is the important agent, although progestins may augment the effect (17-21). The hepatic defect that enhances the effect of estrogens and the pathogenesis of cholestasis remain undefined. These clinical observations stimulated research into the concept that the liver is an important target organ for estrogenic effects and that estrogen-induced cholestasis is an excellent model for study of intrahepatic cholestasis.Recent basic science advances have advanced understanding of the molecular correlates of estrogen effects. Specific estrogen receptors have been demonstrated on plasma membranes (22-23) and in cytosol (24-26), microsomal components (27), and nuclei (25, 28) of hepatocytes in animals. The significance of these receptors is unclear; however, the data suggest that estrogen is transported across the plasma membrane and translocated to the nucleus. Within the nucleus, estrogens bind to DNA (29), stimulate RNA synthesis (30, 31), activate RNA methylating enzymes (32), and inhibit RNA deactivating enzymes (33).Hepatic effects of estrogens are dose-dependent. At the high levels achieved during pregnancy or with ad- ~ ~The authors were supported in part by RCDA (AM-00347) to Francis R. Simon and NIH Training Grant (T32 AM07038-07) to Allen J. Schreiber.

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Urinary excretion of 5-methyltetrahydrofolate and liver S-adenosylmethionine levels of rats fed a vitamin B1 2-deficient diet

Cited by 35 publications

References 21 publications

Effect of Vitamin B₁₂deficiency on phosphatidylethanolamine methylation in rat liver

Effect of Vitamin B₁₂deficiency on phosphatidylethanolamine methylation in rat liver

Obstetric cholestasis

Estrogen-Induced Cholestasis: Clues to Pathogenesis and Treatment

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Urinary excretion of 5-methyltetrahydrofolate and liver S-adenosylmethionine levels of rats fed a vitamin B1 2-deficient diet

Cited by 35 publications

References 21 publications

Effect of Vitamin B12deficiency on phosphatidylethanolamine methylation in rat liver

Effect of Vitamin B12deficiency on phosphatidylethanolamine methylation in rat liver

Obstetric cholestasis

Estrogen-Induced Cholestasis: Clues to Pathogenesis and Treatment

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Product

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Effect of Vitamin B₁₂deficiency on phosphatidylethanolamine methylation in rat liver

Effect of Vitamin B₁₂deficiency on phosphatidylethanolamine methylation in rat liver