Abstract
Corticosterone possesses two distinctly opposite metabolic actions. The actions are strictly dose-dependent and are linked to type I and type II corticosteroid receptor binding. These conclusions are drawn from continuous infusion studies where corticosterone yields a bitonic dose-response curve for body weight gain and feeding efficiency. Anabolic at low serum levels, corticosterone concentrations above 2 ug/dl bring about an opponent catabolic process that intensifies and eventually masks the anabolic action. Relatively pure type I (aldosterone) and type II (RU28362 and dexamethasone) corticosterone receptor agonists produce opposite monotonic functions that respectively mimic the ascending and descending arms of the corticosterone dose-response curve. Stimulation of either receptor increases the proportion of carcass fat to lean body mass by either increasing carcass lipids (type I) or by reducing protein (type II).
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