Metabolic modulators following trauma sepsis: Sex hormones

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Abstract
The development of metabolic perturbations following severe trauma/sepsis leading to decreased energy production, hyperglycemia, and lipolysis is often rapid. Gender is increasingly recognized as a major factor in the outcome of patients suffering from trauma/sepsis. Moreover, sex hormones influence energy, glucose, and lipid metabolism. Metabolic modulators, such as peroxisome proliferator-activated receptor-γ coactivator-1 and peroxisome proliferator-activated receptor-α, which are required for mitochondrial energy production and fatty acid oxidation, are regulated by the estrogen receptor-β and consequently contribute to cardioprotection following trauma hemorrhage. Additionally, sex steroids regulate inflammatory cytokines that cause hypermetabolism/catabolism via acute phase response, leading to increased morbidity and mortality. This article examines the following: (1) the evidence for gender differences; (2) energy, glucose, and lipid metabolism and the acute phase protein response; (3) the mechanisms by which gender/sex hormones affect the metabolic modulators; and (4) the tissue-specific effect of sex hormone receptors and the effect of genomic and nongenomic pathways of sex hormones following trauma. The available information indicates that sex steroids not only modulate the immune/cardiovascular responses but also influence various metabolic processes following trauma. Thus, alteration or modulation of the prevailing hormone milieu at the time of injury appears to be a novel therapeutic adjunct for improving outcome after injury.