This Article
Right arrow Full Text (PDF)
Right arrow Letters to the Editor: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when Letters to the Editor are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
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 Add to My File Cabinet
Right arrow Download to citation manager
Right arrowReprints and Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Brighton, C. T.
Right arrow Articles by Cuckler, J. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Brighton, C. T.
Right arrow Articles by Cuckler, J. M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us   Add to Technorati  
What's this?

The Journal of Bone and Joint Surgery, Vol 65, Issue 5 663-666, Copyright © 1983 by Journal of Bone and Joint Surgery, Inc

JOURNAL CONTENTS

Absence of the glycerol phosphate shuttle in the various zones of the growth plate

CT Brighton, RD Lackman and JM Cuckler

The various zones of the growth plate of the rib of six-week-old male New Zealand White rabbits were obtained by means of a specially devised guillotine slicing apparatus. Cartilage slices from each zone were assayed enzymatically for activity of glycerol phosphate dehydrogenase by an adaptation of a fluorimetric technique based on the conversion of non-fluorescent resazurin to the highly fluorescent resorufin in the presence of nicotinamide adenine dinucleotide and the enzyme. No glycerol phosphate dehydrogenase activity was detectable in any zone of the growth plate, whereas control liver slices exhibited abundant enzyme activity. Thus the glycerol phosphate shuttle, one pathway whereby reducing equivalents are carried or shuttled from cytoplasmic nicotinamide adenine dinucleotide to the intramitochondrial respiratory chain, is entirely lacking in growth-plate chondrocytes. The lack of this enzyme, and the absence of the glycerol phosphate shuttle, may explain the high rate of lactate accumulation in the presence of ample oxygen concentration (aerobic accumulation) even though the Krebs cycle (tricarboxylic acid cycle) and electron transport are proceeding at normal rates. Clinical Relevance: The growth plate is a complex structure whose metabolism is still not well understood. This study demonstrates that, in at least one metabolic pathway, the growth-plate chondrocyte does not resemble other normal cells. Only as we are able to formulate a more complete picture of the metabolism of the normal growth plate will be able to understand, and perhaps correct or prevent, those disease states in which growth-plate metabolism has bone away.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
 FASEB J.Home page
J. WANG, J. ZHOU, and C. A. BONDY
Igf1 promotes longitudinal bone growth by insulin-like actions augmenting chondrocyte hypertrophy
FASEB J, November 1, 1999; 13(14): 1985 - 1990.
[Abstract] [Full Text]