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Abstract

It has been recognized for many years that infection, thermal injury and a variety of traumatic conditions markedly alter substrate utilization. Although the metabolic manifestations of trauma certainly vary with the type and severity of the insult, there are similarities among the responses which may suggest a potential common mechanism. In general, the sepsis- or trauma-induced changes in whole body glucose metabolism are remarkably consistent. These changes include, but are not limited to, normal or slightly elevated plasma glucose levels, elevated lactate concentrations, and enhanced rates of hepatic glucose production and peripheral glucose disposal (Lang et al. 1985; Spitzer et al. 1988). This characteristic glucose metabolic response has been observed in patients and experimental animals which are in the “high flow” or hypermetabolic phase of injury regardless of the etiology (Frayn 1985; Wolfe 1981).

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Lang, C.H. (1993). Mechanism of Insulin Resistance in Infection. In: Schlag, G., Redl, H. (eds) Pathophysiology of Shock, Sepsis, and Organ Failure. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-76736-4_44

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