Document Detail


A regulatory role for cortisol in muscle glycogen metabolism in rainbow trout Oncorhynchus mykiss Walbaum.
MedLine Citation:
PMID:  12909698     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
To test the hypothesis that cortisol has a regulatory role in fish muscle glycogenesis post-exercise, rainbow trout were treated 1 h prior to exercise with either saline (control) or metyrapone (2-methyl-1, 2-di-3-pyridyl-1-propanone) to block cortisol synthesis. Following exercise (time 0), half of the metyrapone-treated fish received a single injection of cortisol, to mimic the post-exercise rise usually observed. Muscle glycogen and the relative activities of glycogen phosphorylase a (Phos a) and glycogen synthase I (GSase I), regulatory enzymes for glycogen resynthesis, were monitored 4 h post-exercise. Metyrapone treatment succeeded in blocking the post-exercise rise in plasma cortisol (17+/-2 vs 118+/-13 ng ml(-1) in controls at time 0), and cortisol injection resulted in a larger and more prolonged cortisol increase than in controls (159+/-22 vs 121+/-14 ng ml(-1) in controls at 1 h). Muscle glycogen was completely restored in the metyrapone-treated fish within 2 h after exercise (8.3+/-0.6 vs 8+/-0.7 micromol g(-1) pre-exercise), only partially restored in control fish at 4 h (5.4+/-01.4 vs 8.8+/-1.3 micromol g(-1) pre-exercise), and not at all in cortisol-treated fish (1.0+/-0.5 micromol g(-1) at 4 h). The rapid glycogen resynthesis in the metyrapone-treated fish was associated with a more rapid inactivation of Phos a and stimulation of GSase I compared to controls. In cortisol-treated fish, Phos a activity persisted throughout 4 h post-exercise; there was also a significant stimulation of GSase I activity. As a consequence of dual activation of Phos a and GSase I, glycogen cycling probably occurred, thus preventing net synthesis. This explains why the post-exercise elevation of cortisol inhibits net glycogen synthesis in trout muscle.
Authors:
C Louise Milligan
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of experimental biology     Volume:  206     ISSN:  0022-0949     ISO Abbreviation:  J. Exp. Biol.     Publication Date:  2003 Sep 
Date Detail:
Created Date:  2003-08-11     Completed Date:  2004-05-24     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0243705     Medline TA:  J Exp Biol     Country:  England    
Other Details:
Languages:  eng     Pagination:  3167-73     Citation Subset:  IM    
Affiliation:
Department of Biology, The University of Western Ontario, London, ON N6A 5B7 Canada. milligan@uwo.ca
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MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Animals
Enzyme Activation / drug effects,  physiology
Glycogen / biosynthesis*,  metabolism
Glycogen Phosphorylase / antagonists & inhibitors,  blood
Glycogen Synthase / blood,  physiology
Hydrocortisone / antagonists & inhibitors,  blood,  metabolism*
Lactic Acid / blood
Metyrapone / pharmacology
Muscle, Skeletal / metabolism*
Oncorhynchus mykiss / metabolism*,  physiology
Physical Exertion / physiology*
Chemical
Reg. No./Substance:
50-21-5/Lactic Acid; 50-23-7/Hydrocortisone; 54-36-4/Metyrapone; 9005-79-2/Glycogen; EC 2.4.1.-/Glycogen Phosphorylase; EC 2.4.1.11/Glycogen Synthase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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