Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1992-8-4
pubmed:abstractText
3-Methylcrotonyl-CoA originates from catabolism of leucine and is normally metabolized to acetyl-CoA. However, in biotin deficiency, reduced hepatic activity of the biotin-dependent enzyme methylcrotonyl-CoA carboxylase causes the enzyme's substrate 3-methylcrotonyl-CoA to be shunted via an alternate pathway to 3-hydroxyisovaleric acid (3-HIA), which is excreted at increased rates in the urine. In a previous study, unequivocal separation in 3-HIA excretion rates between biotin-deficient and control animals was not apparent until d 35 of feeding a diet that induced biotin deficiency. The present study tested the hypothesis that abnormal 3-HIA excretion could be detected earlier in the course of biotin deficiency if 3-HIA were more accurately measured using a method that incorporated an improved extraction regimen, deuterated 3-HIA as internal standard, and unlabeled 3-HIA as external standard. Biotin deficiency was induced in rats by feeding a diet containing avidin; control rats received the same diet and biotin injections. With the more accurate method, unequivocal detection of deficiency was possible in all deficient rats by d 16. This study provides evidence that, in rats, reduction of analytical error allows earlier detection of biotin deficiency and that disturbances of leucine metabolism occur earlier than previously appreciated.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-3166
pubmed:author
pubmed:issnType
Print
pubmed:volume
122
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1493-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Biotin deficiency in rats: disturbances of leucine metabolism are detectable early.
pubmed:affiliation
Department of Pediatrics, University of Iowa College of Medicine, Iowa City 52242.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.