Bile Acid Analyses in “Pseudo-Zellweger” Syndrome; Clues to the Defect in Peroxisomal β-Oxidation View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

1988

AUTHORS

P. T. Clayton , B. D. Lake , M. Hjelm , J. B. P. Stephenson , G. T. N. Besley , R. J. A. Wanders , A. W. Schram , J. M. Tager , R. B. H. Schutgens , A. M. Lawson

ABSTRACT

In Zellweger syndrome, β-oxidation of very long chain fatty acids (VLCFA) and C27 bile acids is impaired because peroxisomes are absent (Schutgens et al., 1986). In 1986, Goldfischer et al. described an infant with ‘pseudo-Zellweger’ syndrome in whom peroxisomes were present but oxidation of VLCFA and C27 bile acids impaired, due to a deficiency of peroxisomal 3-oxoacyl-CoA thiolase (Schram et al., 1987). This paper describes three siblings with deficient peroxisomal β-oxidation but structurally normal peroxisomes. Immunoreactive acyl CoA-oxidase, bifunctional protein and thiolase were all present in the liver but analysis of the C27 bile acids suggested a functional deficiency of peroxisomal thiolase (or possibly of the bifunctional protein). More... »

PAGES

165-168

References to SciGraph publications

Book

TITLE

Studies in Inherited Metabolic Disease

ISBN

978-94-010-7059-1
978-94-009-1259-5

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-94-009-1259-5_22

DOI

http://dx.doi.org/10.1007/978-94-009-1259-5_22

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1016229885


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