RESUMO
AbstractThe stress response is partially mediated by increased levels of circulating glucocorticoids. While the stress response may be adaptive in the short term, chronically elevated levels of glucocorticoids can be pathological. We aimed to verify that chronic stress causes metabolic dysregulation via increased corticosterone (Cort) exposure by monitoring free fatty acid (FFA) concentrations (evidence of fat breakdown), uric acid concentrations (evidence of protein breakdown), and organ weights (furcular fat, abdominal fat, liver, and pectoralis muscle) in chronically stressed juvenile house sparrows (Passer domesticus). The sparrows were chronically stressed for 3 wk by applying a series of rotating mild psychological stressors. One group of birds received injections of a glucocorticoid steroidogenesis inhibitor (mitotane) and a second group received injections of a glucocorticoid receptor antagonist (RU486) halfway through the chronic stress period to test whether glucocorticoids are responsible for protein and fat catabolism during chronic stress. Toward the end of the chronic stress period, mitotane birds increased weight compared to control and RU486 birds. Contrary to expectations, we saw no differences in FFA or uric acid levels between control and mitotane birds, but RU486 temporarily decreased stress-induced uric acid levels. Neither mitotane nor RU486 significantly altered organ weights at the end of the 3 wk. In conclusion, Cort does appear to negatively affect body weight, but the mechanism does not appear to involve increased protein or lipid metabolism.