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Riboflavin deficiency and β‐oxidation systems in rat liver
Author(s) -
Sakurai Takehiko,
Miyazawa Shoko,
Furuta Shuichi,
Hashimoto Takashi
Publication year - 1982
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/bf02535365
Subject(s) - clinical chemistry , riboflavin , lipidology , chemistry , biochemistry , environmental chemistry
Abstract Weanling rats were fed a riboflavin‐deficient diet. The mitochondrial fatty acid oxidation in liver was depressed in riboflavin deficiency but restored after supplementation of riboflavin. Among the enzymes involved in this system, only the acyl‐CoA dehydrogenase (EC 1.3.99.2 and 1.3.99.3) activities varied with the change in fatty acid oxidation. An accumulation of the apoforms of acyl‐CoA dehydrogenases was found in riboflavin deficiency. The levels of electron transfer flavoprotein and other enzymes involved in the β‐oxidation system remained unchanged. The peroxisomal fatty acid oxidation and levels of individual enzymes of this system remained constant. No accumulation of the apoform of acyl‐CoA oxidase was observed under simple, riboflavin‐deficient conditions. However, accumulation of a large amount of apo‐acyl‐CoA oxidase was observed when the peroxisomal system was induced by administration of a peroxisome proliferator, di(2‐ethylhexyl)phthalate, under riboflavin‐deficient conditions.