Homocysteine metabolism.

@article{Selhub1999HomocysteineM,
  title={Homocysteine metabolism.},
  author={Jacob Selhub},
  journal={Annual review of nutrition},
  year={1999},
  volume={19},
  pages={
          217-46
        }
}
  • J. Selhub
  • Published 1999
  • Medicine
  • Annual review of nutrition
Homocysteine is a sulfur amino acid whose metabolism stands at the intersection of two pathways: remethylation to methionine, which requires folate and vitamin B12 (or betaine in an alternative reaction); and transsulfuration to cystathionine, which requires pyridoxal-5'-phosphate. The two pathways are coordinated by S-adenosylmethionine, which acts as an allosteric inhibitor of the methylenetetrahydrofolate reductase reaction and as an activator of cystathionine beta-synthase… 
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The focus of this review is to study existing literature on HHcy and its role in relation to DNA methylation, which includes studies which were conducted in animal models as well as humans.
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This manuscript sums up the findings from the laboratory and public database regarding genetics of HHcy and its effects on ocular disorders, their respective management during dysregulation of the 1-carbon metabolism.
One-carbon cycle alterations induced by Dyrk1a dosage
TLDR
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TLDR
Two different forms of the disease can be primarily as a universal methyl donor to a variety of acdistinguished on the basis of the responsiveness to treatment ceptors including guanidinoacetate, nucleic acids, neurowith large dosages of vitamin B6.
Deranged B12 metabolism: Effects on sulfur amino acid metabolism
Abstract Several enzymes have been studied in the tissues of a patient who had a combination of increased homocystine and cystathionine and decreased methionine in plasma, tissues, and urine. This
Folate-deficiency-induced homocysteinaemia in rats: disruption of S-adenosylmethionine's co-ordinate regulation of homocysteine metabolism.
TLDR
Plasma homocysteine and hepatic AdoMet concentrations were inversely correlated as folate status was modified, and the effect of ethionine is thought to be exerted through S-adenosylethionine, which is formed in the liver of these rats.
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TLDR
This work has identified a common mutation in MTHFR which alters a highly-conserved amino acid; the substitution occurs at a frequency of approximately 38% of unselected chromosomes and may represent an important genetic risk factor in vascular disease.
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TLDR
Individuals with thermolabile MTHFR may have a higher folate requirement for regulation of plasma homocysteine concentrations; folate supplementation may be necessary to prevent fasting hyperhomocysteinemia in such persons.
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TLDR
Using an in vitro system which contained enzymes, substrates, and other reactants at concentrations which approximated the in vivo conditions in rat liver, it was demonstrated that the adaptation from a high protein diet to a low protein diet is achieved by a significant increase in betaine homocysteine methyltransferase, and 83% reduction in cystathionine synthase, which contributes significantly to the regulation of the pathway.
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TLDR
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TLDR
The novelty of the hypothesis is the assertion that impairment of one homocysteine metabolic pathway must lead to the impairment of the otherhomocysteines metabolic pathway to cause homocysteinemia, which extends the simplistic view that a block of only one of the pathways is sufficient to cause Homocysteemia.
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TLDR
Seven novel mutations in this gene are characterized: six missense mutations and a 5' splice-site defect that activates a cryptic splice site in the coding sequence that is associated with extremely low activity and onset of symptoms within the 1st year of age.
Elevated total plasma homocysteine and 677C-->T mutation of the 5,10-methylenetetrahydrofolate reductase gene in thrombotic vascular disease.
TLDR
Preliminary evidence indicates that the frequency of homozygotes for the 677C{r_arrow}T mutation may vary significantly in populations from different geographic areas.
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