Systemic inflammation contributes to the development of multiple organ dysfunction, the major cause of mortality in patients with septic shock. Systemic inflammation is a consequence of activation of the innate immune system. Recent studies have indicated that adipose tissue plays a major role in the secretion of inflammatory factors, which have been called adipo-cytokines or adipokines.
Also, the increased production rate of cytokines such as IL-6 or TNF-alpha has been implicated in the pathogenesis of car diovascular complications and insulin resistance. However, the metabolic role and possible consequences of adipose tissue as a secretory organ in critically ill patients has not been investigated to date. For the present proposal we will test the hypothesis, that adipose tissue is one of the links between systemic inflammation causing insulin resistance in critically ill patients and low-grade inflammation causing insulin resistance in obesity. To test this obesity we will characterize adipose tissue as a secretory organ using interstitial fluid sampling techniques and advanced peptide analysis in critically ill patients and healthy controls.
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