Stress and sepsis induce a hypermetabolic state of increased energy expenditure and increased loss of urinary nitrogen. This hypermetabolic state is found routinely in patients with burn injury, trauma injury, infection, etc., yet our understanding of what produces this state is weak. The magnitude of the hypermetabolic state can be related to the severity of the injury, and changes in levels of hormones and other mediators have been characterized. Studies in normal healthy humans have defined several key factors which influence the hypermetabolic state. Epinephrine is a catecholamine which has been well studied in terms of its metabolic effects of increasing metabolic rate and altering amino acid levels. Catecholamines are routinely elevated in injured and stressed subjects. However, the role of the catecholamines in producing the hypermetabolic state of injury has not been completely characterized. There are several important aspects of epinephrine's metabolic action in humans which need to be clarified. The long term goals of this proposal are to characterize in normal humans what the metabolic effects of hormones, such as epinephrine, have in terms of energy and protein metabolism. Results from these studies will be used to design in vitro studies which may elucidate how this regulation occurs. Our approach has been to administer stable isotopically labeled tracers to determine amino acid, glucose and fat kinetics in healthy individuals. This proposal has 3 aims: (1) To define how epinephrine acutely alters and regulates amino acid metabolism in humans. (2) To define whether the effect of epinephrine in increasing metabolic rate is transient or whether epinephrine will chronically elevate energy expenditure. (3) To define which metabolic fuels are used by the body when epinephrine induces a chronic increase in metabolic rate. These studies are relevant to injury and trauma where patients typically have elevated catecholamine levels and in patients suffering chronic stress.
| Ratheiser, K M; Pesola, G R; Campbell, R G et al. (1999) Epinephrine transiently increases amino acid disappearance to lower amino acid levels in humans. JPEN J Parenter Enteral Nutr 23:279-87 |
| Ratheiser, K M; Brillon, D J; Campbell, R G et al. (1998) Epinephrine produces a prolonged elevation in metabolic rate in humans. Am J Clin Nutr 68:1046-52 |
