GLUCOCORTICOIDS AND ACIDOSIS STIMULATE PROTEIN AND AMINO-ACID CATABOLISM IN-VIVO

We have shown that chronic metabolic acidosis in awake rats accelerate s whole body protein turnover using stochastic modeling and a continuo us infusion of L-[1-C-13] leucine. To delineate the role that glucocor ticoids play in mediating these catabolic responses, we measured prote in turnover in awake, chronically catheterized, adrenalectomized rats in the presence or absence of glucocorticoids and/or a NH4Cl feeding r egimen which induced chronic metabolic acidosis. In adrenalectomized r ats receiving no glucocorticoids there was no statistical difference i n amino acid oxidation, protein degradation or synthesis whether or no t the rats had acidosis. In contrast, chronically acidotic, adrenalect omized rats receiving glucocorticoids demonstrated accelerated whole b ody protein turnover with a 84% increase in amino acid oxidation and a 26% increase in protein degradation, compared to rats not receiving g lucocorticoids or those given the same dose of glucocorticoids but wit hout acidosis. We conclude that metabolic acidosis accelerates amino a cid oxidation and protein degradation in vivo, and that glucocorticoid s are necessary but not sufficient to mediate the catabolic effects of metabolic acidosis.