RESUMO
BACKGROUND: Postburn insulin dysfunction is a significant contributor to morbidity and mortality. A satisfactory mechanism for explaining this phenomenon remains elusive; however, resistin has been postulated to be involved. Initially discovered as an insulin antagonist secreted from adipose tissue in murine models, resistin's function in humans has been more obscure. Resistin is not expressed significantly in human adipocytes although it has been detected in monocytes. We postulate that mononuclear activation at the site of burn injury affects the release of resistin and contributes to insulin dysfunction. METHODS: Plasma from burned and healthy control individuals was characterized for glucose, insulin, and resistin protein levels. Adipose tissue from both groups was analyzed for resistin transcript; levels were found to be somewhat higher in the burned group though not significantly so. Circulating monocyte expression of resistin transcript was assayed in similar fashion. RESULTS: In addition to finding that insulin and glucose were elevated postburn, a finding in agreement with past studies, we demonstrate that circulating resistin levels are significantly elevated as well. Insulin resistance was found to increase at a similar rate to resistin expression in the burn population, suggesting a correlation in these events. Adipose tissue from both groups was analyzed for resistin transcript; levels were found to be somewhat higher in the burned group though not significantly so. Circulating monocyte expression of resistin transcript was assayed and found to be profoundly elevated in the burn population. CONCLUSIONS: This data suggests that resistin is produced by activated monocytes in the adipose tissue around the periphery of burn wound. We suggest that postburn insulin function is adversely affected by resistin produced as a result of this monocyte activation.
