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OtherCARDIOVASCULAR PHARMACOLOGY

Influence of Oral S-Adenosylmethionine on Plasma 5-Methyltetrahydrofolate, S-Adenosylhomocysteine, Homocysteine and Methionine in Healthy Humans

Franziska M. T. Loehrer, Roger Schwab, Christian P. Angst, Walter E. Haefeli and Brian Fowler
Journal of Pharmacology and Experimental Therapeutics August 1997, 282 (2) 845-850;
Franziska M. T. Loehrer
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Roger Schwab
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Christian P. Angst
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Walter E. Haefeli
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Brian Fowler
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Abstract

Elevated plasma homocysteine concentration is an independent risk factor for vascular disease in humans. In addition to nutritional and genetic factors, an interruption of the coordinate regulatory function of S-adenosylmethionine has been proposed to be involved in the occurrence of hyperhomocysteinemia. The effect of oral S-adenosylmethionine on homocysteine metabolism in humans is unknown. We investigated the effect of oral S-adenosylmethionine (400 mg) on plasma levels of 5-methyltetrahydrofolate, which is the active form of folate in the remethylation of homocysteine to methionine, S-adenosylhomocysteine, the demethylated product of S-adenosylmethionine, homocysteine and methionine over 24 hr in 14 healthy subjects. After oral administration, S-adenosylmethionine increased from 38.0 ± 13.4 to 361.8 ± 66.4 nmol/liter (mean ± S.E., P < .001) and returned to base-line values with a half-life of 1.7 ± 0.3 hr. Both S-adenosylhomocysteine and 5-methyltetrahydrofolate showed a significant transient increase (from 29.9 ± 3.7 to 51.7 ± 7.1 nmol/liter, and from 25.1 ± 2.5 to 36.2 ± 3.5 nmol/liter, respectively, P < .001), although homocysteine and methionine did not change over the time of measurement. These changes were not found in subjects without previous S-adenosylmethionine administration. The observed metabolic changes suggest that S-adenosylmethionine, at least in concentrations obtained in this study, does not inhibit 5,10-methylenetetrahydrofolate reductase, the 5-methyltetrahydrofolate forming enzyme. Rather they indicate a positive effect on 5-methyltetrahydrofolate, a key cofactor in homocysteine metabolism, which should be considered in homocysteine lowering strategies for the prevention of vascular disease.

Footnotes

  • Send reprint requests to: Dr. Brian Fowler, University Children’s Hospital Basel, Metabolic Unit, CH-4005 Basel, Switzerland.

  • ↵1 This study was supported by Grants 3200-039439.93 from the Swiss National Science Foundation; the Treubel Foundation, Basel; F. Hoffmann-La Roche Ltd., Vitamins and Fine Chemicals Division Exploratory Research, Basel, Switzerland; and from BioResearch Spa, Liscato, Italy.

  • Abbreviations:
    methyleneTHF
    5,10-methylenetetrahydrofolate
    MeTHF
    5-methyltetrahydrofolate
    AdoMet
    S-adenosylmethionine
    AdoHcy
    S-adenosylhomocysteine
    Cbl
    cobalamin
    PLP
    pyridoxal phosphate
    THF
    tetrahydrofolate
    MS
    5-methyltetrahydrofolate-homocysteine methyltransferase (methionine synthase)
    CO
    base-line concentration
    Cmax
    peak or trough concentration
    tmax
    time to reach Cmax
    ΔC
    difference between CO and the concentration at a specific time of sampling
    AUC
    area under the concentration-time curve
    BW
    body weight
    • Received August 26, 1996.
    • Accepted April 14, 1997.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics
Vol. 282, Issue 2
1 Aug 1997
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OtherCARDIOVASCULAR PHARMACOLOGY

Influence of Oral S-Adenosylmethionine on Plasma 5-Methyltetrahydrofolate, S-Adenosylhomocysteine, Homocysteine and Methionine in Healthy Humans

Franziska M. T. Loehrer, Roger Schwab, Christian P. Angst, Walter E. Haefeli and Brian Fowler
Journal of Pharmacology and Experimental Therapeutics August 1, 1997, 282 (2) 845-850;

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OtherCARDIOVASCULAR PHARMACOLOGY

Influence of Oral S-Adenosylmethionine on Plasma 5-Methyltetrahydrofolate, S-Adenosylhomocysteine, Homocysteine and Methionine in Healthy Humans

Franziska M. T. Loehrer, Roger Schwab, Christian P. Angst, Walter E. Haefeli and Brian Fowler
Journal of Pharmacology and Experimental Therapeutics August 1, 1997, 282 (2) 845-850;
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