Glucocorticoids and acidosis stimulate protein and amino acid catabolism in vivo

• Published in: Kidney international Vol. 49; no. 3; pp. 679 - 683
• Main Authors: May, Robert C., Bailey, James L., Mitch, William E., Masud, Tahsin, England, Brian K.
• Format: Journal Article Conference Proceeding
• Language: English
• Published: New York, NY Elsevier Inc 01-03-1996; Nature Publishing
• Subjects: Acidosis - metabolism; Adrenalectomy; Amino Acids - drug effects; Amino Acids - metabolism; Animals; Biological and medical sciences; Chronic Disease; Dexamethasone - pharmacology; Glucocorticoids - pharmacology; Male; Medical sciences; Metabolic diseases; Miscellaneous; Other metabolic disorders; Proteins - drug effects; Proteins - metabolism; Random Allocation; Rats; Rats, Sprague-Dawley; Rat; Steroid hormone; Rodentia; Acid base balance disorder; Metabolism; Glucocorticoid; Proteins; In vivo; Vertebrata; Mammalia; Aminoacid; Animal; Adrenal hormone; Catabolism; Oxidation; Metabolic acidosis
• ISSN: 0085-2538; 1523-1755
• DOI: 10.1038/ki.1996.96

Glucocorticoids and acidosis stimulate protein and amino acid catabolism in vivo. We have shown that chronic metabolic acidosis in awake rats accelerates whole body protein turnover using stochastic modeling and a continuous infusion of L-[1-13C] leucine. To delineate the role that glucocorticoids play in mediating these catabolic responses, we measured protein turnover in awake, chronically catheterized, adrenalectomized rats in the presence or absence of glucocorticoids and/or a NH4Cl feeding regimen which induced chronic metabolic acidosis. In adrenalectomized rats receiving no glucocorticoids there was no statistical difference in amino acid oxidation, protein degradation or synthesis whether or not the rats had acidosis. In contrast, chronically acidotic, adrenalectomized rats receiving glucocorticoids demonstrated accelerated whole body protein turnover with a 84% increase in amino acid oxidation and a 26% increase in protein degradation, compared to rats not receiving glucocorticoids or those given the same dose of glucocorticoids but without acidosis. We conclude that metabolic acidosis accelerates amino acid oxidation and protein degradation in vivo, and that glucocorticoids are necessary but not sufficient to mediate the catabolic effects of metabolic acidosis.