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Metabolic effects associated with chronically elevated cortisol in rainbow trout (Oncorhynchus mykiss).

The metabolic role of chronically elevated cortisol in otherwise unstressed rainbow trout, Oncorhynchus mykiss, was examined. Fish were fitted with mini-osmotic pumps which maintained plasma cortisol levels at approximately 100 or 200 ng $\cdot$ mL$\sp{-1}$ for ten days. Plasma metabolites, liver enzyme activities, liver glycogen content, metabolic flux in isolated hepatocytes and alanine turnover were investigated. Plasma glucose, lactate and protein levels were unaffected by ten days of cortisol administration, despite a significant elevation in plasma cortisol. Plasma amino acids in cortisol treated fish (1023.8 $\pm$ 90.7 $\rm\mu g\cdot mL\sp{-1})$ were significantly elevated compared to shams $\rm(716.7\pm68.5\ \mu g\cdot mL\sp{-1})$ after nine days. Liver glycogen content was significantly reduced by cortisol treatment. The activities of the liver enzymes assayed were unchanged; likewise the fluxes of radioactive substrates to radiolabelled CO$\sb2,$ glucose, and protein in isolated hepatocytes were unaffected in trout with chronically elevated cortisol compared to shams. Both the caloric and water contents of white muscle were unaffected by chronically elevated circulating cortisol levels. The cortisol treatment did not alter the turnover of alanine. These data do not support the purported role of cortisol as a glucocorticoid in rainbow trout. While chronically elevated cortisol may increase the supply of plasma amino acids, the hormone does not appear to alter the manner in which these potential gluconeogenic substrates are metabolized. The absence of other stressors may be partially responsible for the differences between this study and others in the literature.

Identiferoai:union.ndltd.org:uottawa.ca/oai:ruor.uottawa.ca:10393/7714
Date January 1993
CreatorsAndersen, Donald E.
ContributorsMoon, Tom,
PublisherUniversity of Ottawa (Canada)
Source SetsUniversité d’Ottawa
Detected LanguageEnglish
TypeThesis
Format102 p.

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