Stress induces a hypermetabolic state of increased urinary nitrogen loss and increased metabolic rate. The principal reason for such a response is the mobilization of amino acids and the production of glucose to provide energy for the cells involved in the host immune response and wound repair. The endocrine hormones, eg, cortisol, the catecholamines, and glucagon, are largely responsible for these effects. Insulin and growth hormone administration can produce anabolic effects to block the loss of body protein. Administration of specific amino acids, such as glutamine, also appears to be beneficial. However, the hypermetabolic state goes beyond derangement of endocrine hormone levels. Although the cytokines are also important mediators, it is not clear how these mediators, in concert with hormonal changes, produce all of the manifestations of the hypermetabolic state seen in stress.