Identification of the hepatic insulin and catecholamine signalling pathway after major trauma

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The systemic inflammatory response after trauma leads to hypermetabolism and thus protein degradation and catabolism. As a consequence the structure and function of essential organs, such as the muscle, skin, heart, immune system and liver are compromised and contribute to multi organ failure and mortality. Pro-inflammatory mediators such as pro-inflammatory signal transcription factors, cytokines and acute-phase-proteins were thought to trigger and enhance this response and to mediate the catabolic effects, e.g. by the inhibition of the growth hormone-insulin-like growth factor-I (IGF-I)-insulin axis. After the clinical failure of anti-inflammatory agents or antibodies against pro-inflammatory cytokines such as tumor necrosis (TNF), interleukin-1b (IL-1b), or their receptors, different approaches were taken to attenuate hypermetabolism, one of which being the application of anabolic growth factors. It has been recently shown that insulin and beta blocker (e.g. propanolol) are possible agents to attenuate hypermetabolism, thus each cellular signalling pathway is of major importance. The hepatic cellular signal transcription pathway of insulin and catecholamine after major trauma and a consecutive incidence of sepsis are not entirely defined. Therefore the aim of the present study is to determine the insulin and catecholamine signal transcription pathway after a burn injury and consecutive onset of sepsis, and whether a catecholamine blocking agent (e.g. propanolol) and/or insulin modulate hepatic hypermetabolism and the immune response, thus representing a potential therapeutic approach.