Meeting Abstract
Glucocorticoid release following acute stress causes metabolic alterations that facilitate the response to, and recovery from, immediate stress. Repeated or chronic stress, however, can result in persistent activation of the stress response with maladaptive consequences. We investigated the metabolic consequences to repeated stress in a well-studied marine mammal, the northern elephant seal, by repeated administration of ACTH over four consecutive days. Blood samples were collected for eight hours following ACTH administration on days 1 and 4 to characterize the acute and chronic responses, respectively. The metabolic response to stress was assessed using non-targeted metabolomics. 388 biochemicals were detected; of these, 281 compounds of multiple classes (e.g. lipids, amino acids) showed a significant change during the study (p+q<0.05), suggesting a wide-ranging metabolic response. Stress induction was associated with lipid mobilization, evidenced by increased concentrations of circulating free fatty acids. The magnitude of the circulating lipid response was greater in the acute than in the chronic stress state (p<0.05). Several amino acids (e.g. alanine, lysine, tyrosine) declined during the stress response (p<0.05); without a related increase in TCA cycle or urea cycle intermediates, suggesting either reduced protein catabolism or increased amino acid uptake and resynthesis. Thus, glucocorticoid release may be associated with protein conservation in this fasting adapted species. No single biochemical was unique to acute or chronic stress, but patterns of biochemicals might be useful indicators that distinguish between acute and chronic stress states in this and potentially other species.
