Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2001-1-26
pubmed:abstractText
Proton NMR spectra of urine from subjects with multiple acyl-CoA dehydrogenase deficiency, caused by defects in either the electron transport flavoprotein or electron transport flavoprotein ubiquinone oxidoreductase, provide a characteristic and possibly diagnostic metabolite profile. The detection of dimethylglycine and sarcosine, intermediates in the oxidative degradation of choline, should discriminate between multiple acyl-CoA dehydrogenase deficiency and related disorders involving fatty acid oxidation. The excretion rates of betaine, dimethylglycine (and sarcosine) in these subjects give an estimate of the minimum rates of both choline oxidation and methyl group release from betaine and reveal that the latter is comparable with the calculated total body methyl requirement in the human infant even when choline intake is very low. Our results provide a new insight into the rates of in vivo methylation in early human development.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0006-3002
pubmed:author
pubmed:copyrightInfo
Copyright 1998 Elsevier Science B.V. All rights reserved.
pubmed:issnType
Print
pubmed:day
28
pubmed:volume
1406
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
274-82
pubmed:dateRevised
2010-8-25
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Proton NMR spectroscopic analysis of multiple acyl-CoA dehydrogenase deficiency--capacity of the choline oxidation pathway for methylation in vivo.
pubmed:affiliation
Medical Unit, Cellular and Molecular Mechanisms Research Group, St. Bartholomew's and The Royal London School of Medicine and Dentistry, Whitechapel, London E1 1BB, UK.
pubmed:publicationType
Journal Article, Case Reports, Research Support, Non-U.S. Gov't