Abstract
The metabolic impact of infectious, neoplastic and certain other disease states have long been known to clinicians. Those diseases in general induce, aside specific symptoms associated with the disease itself, general signs and symptoms [1]. These alterations include fever, hypermetabolism, cachexia, leukocytosis, hypo-ferremia and marked changes in carbohydrate-, protein- and lipid metabolism, resulting in hyperglycemia, sometimes followed by hypoglycemia, increased glucose production, protein catabolism, hypertriglyceridemia, increased free fatty acid (FFA) turnover and decreased ketonemia [2, 3]. It was once believed that these metabolic derangements were induced by the disease itself and that differences in the metabolic response were due to differences between disease states. In recent years however, there has been a growing awareness that the metabolic responses to disease tend to occur in a consistent and predictable manner and that endogenous mediators could be essential elements in the pathogenesis of above-mentioned responses [1, 3, 4]. Some of these mediators, the “classical” hormones are well-known for a longtime: corticosteroids, catecholamines, glucagon, growth-hormone and insulin. The accepted explanation for the changes in glucose-, protein-, and fat metabolism were marked increases in the plasma concentrations of the counter-regulatory hormones together with decreased tissue sensitivity to insulin [2]. These explanations have been substantiated by recent studies [3]. In healthy volunteers was shown that hypermetabolism, hyperglycemia, but not hypoglycemia, protein loss and increased lipolysis can be induced by the infusion of the counter-regulatory hormones. Simultaneous infusion of these hormones was necessary, as separate infusion of each of them provided lesser and sometimes only transient metabolic changes. These metabolic changes however are sometimes also seen despite seemingly normal plasma concentrations of the counter-regulatory hormones [5] whereas other metabolic responses like fever, acute phase protein synthesis, hypoferremia and leukocytosis could be induced only by injection of an inflammatory agent like etiocholanon [3, 4].
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Keywords
- Rest Energy Expenditure
- Human Immune Deficiency Virus
- Insulin Clearance
- Recombinant Human Tumor Necrosis Factor
- Human Immune Deficiency Virus Infection
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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© 1991 Springer-Verlag Berlin, Heidelberg
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Sauerwein, H.P., van der Poll, T., Romijn, J.A. (1991). Cytokines: Role in Human Metabolism. In: Vincent, J.L. (eds) Update 1991. Update in Intensive Care and Emergency Medicine, vol 14. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-84423-2_29
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DOI: https://doi.org/10.1007/978-3-642-84423-2_29
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