Journal of Nutrition LabDiet, Your World of Nutritional Answers

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Shriver, B. J.
Right arrow Articles by Allred, J. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Shriver, B. J.
Right arrow Articles by Allred, J. B.

Depletion and Repletion of Biotinyl Enzymes in Liver of Biotin-Deficient Rats: Evidence of a Biotin Storage System1,2,

Brent J. Shriver3, Carmen Roman-Shriver4 and John B. Allred5

Laboratory of Metabolic Regulation, Department of Food Science and Technology, The Ohio State University, Columbus, OH 43210

The quantities of biotinyl proteins in liver of young rats were compared with age-matched controls at intervals during depletion and repletion of biotin. Growth rate and the concentrations of biotinyl proteins previously proposed as mitochondrial storage forms of acetyl CoA carboxylase rapidly decreased in response to biotin deprivation, whereas neither the concentration nor activity of cytosolic acetyl CoA carboxylase was affected. Concentrations of carboxylases active within mitochondria (pyruvate carboxylase, propionyl CoA carboxylase and 3-methyl crotonyl CoA carboxylase) decreased only after d 28. When biotin was injected into biotin-deficient rats, concentrations of the carboxylases active within mitochondria were restored to control levels within 3 h, whereas the concentrations of putative mitochondrial storage forms of acetyl CoA carboxylase reached normal levels only after 9 h, indicating that the injected biotin was preferentially used for the synthesis of the carboxylases active within mitochondria rather than acetyl CoA carboxylase. Mitochondrial acetyl CoA carboxylase may serve as a reservoir to maintain a normal concentration of cytosolic acetyl CoA carboxylase in liver of rats deprived of biotin and provide biotin, indirectly, to maintain essentially normal concentrations of the biotinyl enzymes active within mitochondria for several weeks after rats were fed a biotin-deficient diet.


KEY WORDS: • biotin deficiency • biotin repletion • biotin enzyme concentrations • rats • biotin storage mechanism

1 Support for this work was provided by state and federal funds appropriated to the Ohio Agricultural Research and Development Center, The Ohio State University, Columbus, OH, and by National Institutes of Health grant no. HD23352. Journal article 22-93.

2 The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

3 Current address: Robert Dowben Associates, Inc., 2170 Lone Star Drive, Dallas, TX 75212.

4 Current address: Department of Nutrition and Food Science, Texas Woman's University, Denton, TX 76204.

5 To whom correspondence should be addressed.

Manuscript received 3 November 1992. Revision accepted 2 February 1993.







Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
Copyright © 1993 by American Society for Nutrition