Abstract
The critically ill septic patient often exhibits profound and accelerated signs of nutritional deficiency. Hypermetabolism, wasting with nitrogen loss, hypoalbuminemia, increased levels of acute-phase proteins, hyperglycemia, hyperlipidemia and intolerance to nutrients have all been observed [1]. However, the ability to nourish these patients is often hindered because of altered nutrient metabolism [2]. It is now increasingly being recognized that cytokines [3], especially cachectin (TNF) [4], interleukin-1 (IL-1) and IL-6, are either associated with sepsis or are the mediators of a number of metabolic phenomena observed in sepsis [5-15], including anorexia, fever, hypotension, somnolence, acute-phase protein synthesis, abnormalities of lipid and glucose metabolism. Sepsis is often associated with malnutrition, and TNF as well as IL-6 have been shown to cause wasting due to metabolic effects and/or anorexia [12,13,16–21]. However it should be recognized that TNF can induce the production of both IL-1 and IL-6 [22,23]. In clinical sepsis, the release of hormones in response to shock and endotoxin may add to the metabolic events.
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References
Beisel WR (1984) Nutrition, infection, specific immune responses and nonspecific host defenses: A complex interaction. In: Matson RR (eds) Nutrition, Disease Resistance, and Immune Function. New York Marcel Dekker pp 3–34
Fischer JE, Freund HR (1983) Central Hyperalimentation. In: Fischer JE (ed) Surgical Nutrition Little, Brown and Co. Boston, MA pp 663–702
Dinarello CA, Mier JW (1987) Current concepts: Lymphognes. N Engl J Med 317: 940–945
Beutler B, Cerami A (1986) Cachectin and tumor necrosis factor as two sides of the same biological coin. Nature 320: 584–588
Cerami A, Ikeda Y, Trang NLE, Hotez PJ, Beutler B (1985) Weight loss associated with an endotoxin-induced mediator from peripheral macrophages: The role of cachectin (tumor necrosis factor) Immunol (Lett) 11: 173–177
Oliff A, Defeo-Jones D, Boyer M, et al. (1987) Tumors secreting human TNF/cachectin induce cachexia in mice. Cell 50: 555–563
Dinarello CA, Cannon JG, Wolff SM, et al. (1986) Tumor necrosis factor (cachectin) is an endogenous pyrogen and induces production of interleukin-1. J Exp Med 163: 1433–1450
Torti FM, Dieckmann B, Beutler B, Cerami A, Ringold GM (1985) A macrophage factor inhibits adipocyte gene expression: An in vitro model of cachexia. Science 229: 867–869
Perlmutter DH, Dinarello CA, Punsal PI, Colten HR (1986) Cachectin/tumor necrosis factor regulates hepatic acute-phase gene expression. J Clin Invest 78: 1349–1354
Lee MD, Zentella A, Pekala PH, and Cerami A (1987) Effect of endotoxin–induced monokines on glucose metabolism in muscle cell line L6. Proc Natl Acad Sei USA 84: 2590–2594
Shoham S, Davenne D, Cady AB, Dinarello CA, Krueger JM (1987) Recombinant tumor necrosis factor and interleukin 1 enhance slow-wave sleep. Am J Physiol 253: 142–149
Flores EA, Bistrian BR, Pomposelli JJ, Dinarello CA, Blackburn GL, Istfan NW (1989) Infusion of tumor necrosis factor/cachectin promotes muscle catabolism. A synergistic effect of interleukin 1. J Clin Invest 83: 1614–1622
Fong Y, Moldawer LL, Marano M et al. (1989) Cachectin/TFN or IL-1 alpha induces cachexia with redistribution of body protein. Am J Physiol 256: 659–665
Billiar TR, Curran RD, Williams DL, Kispert PH (1992) Liver nonparenchymal cells are stimulated to provide interleukin 6 for induction of hepatic acute-phase response in endotoxemia but not in remote localized inflammation. Arch Surg 127: 31–36
Schuter B, Konig B, Bergman U, Muller FE and Konig W (1991) Interleukin 6 — a potential mediator of lethal sepsis after major thermal trauma: evidence for increased IL–6 production by peripheral blood mononuclear cells. J Trauma 31: 1663–1670
Strassmann G, Fond M, Kenney JS, Jacob CH (1992) Evidence for the involvement of interleukin 6 in experimental cancer cachexia. J Clin Invest 89: 1681–1684
Tracey KJ, Wei H, Manogue KR, et al. (1988) Cachectin/Tumor necrosis factor induced cachexia, anemia and inflammation. J Exp Med 167: 1211–1227
Mahoney SM, Tisdale MJ (1988) Induction of weight loss and metabolic alterations by human recombinant tumor necrosis factor. Br J Cancer 58: 345–349
Warren RS, Starnes HF, Gabrilove JL, Oettgen HF, Brennan MF (1987) The acute metabolic effects of tumor necrosis factor administration. Arch Surg 122: 1396–1400
Kettlehut, IC, Goldberg AL (1988) Tumor necrosis factor can induce fever in rats without activating protein breakdown in muscle or lipolysis in adipose tissue. J Clin Invest 81: 1384–1389
Michie HR, Sherman ML, Spriggs DR, Rounds J, Christie M, Wilmore DW (1989) Chronic TNF infusion causes anorexia but not accelerated nitrogen loss. Ann Surg 209: 19–24
Dinarello DA, Cannon JG, Wolff SM, et al. (1986) Tumor necrosis factor (cachectin) is an endogenous pyrogen and induces production of interleukin 1. J Exp Med 163: 1433–1450
Zhang YH, Lin JX, Vilcek J (1990) Interleukin-6 induction by tumor necrosis factor and interleukin-1 in human fibroblasts involves activation of a nuclear factor binding to a kappa B-like sequence. Mol Cell Biol 10: 3818–3823
Tracey KJ, Morgello S, Kopiin B, et al. (1990) Metabolic effects of cachectin/tumor necrosis factor are modified by site of production. J Clin Invest 86: 2014–2024
Hoshino E, Pichard C, Greenwood CE, et al. (1991) Body composition and metabolic rate in rat during a continuous infusion of cachectin. Am J Physiol 260: E27–E36
Wurtman RJ, Hefti F, Melamed G (1981) Precursor control of neurotransmitter synthesis. Pharmacol Rev 32: 315–335
Conlay LA, Zeisel SH (1982) Neurotransmitter precursors and brain function. Neurosurgery 10: 524–529
Kaye WH, Ebert MH, Gwirtsman HE, Weiss SR (1984) Differences in brain serotonergic metabolism between nonbulimic and bulimic patients with anorexia nervosa. Am J Psychiatry 141: 1598–1601
Hartmann E (1983) Effects of L-tryptophan on sleepiness and sleep. J Psychiat Res 17: 107–114
Fong Y, Marano MA, Moldawer LL, et al. (1990) The acute splanchnic and peripheral tissue metabolic response to endotoxin in humans. J Clin Invest 85: 1896–1904
Michie HR, Spriggs DR, Monague KR, et al. (1988) Tumor necrosis factor and endotoxin induce similar metabolic responses in human beings. Surgery 104: 280–286
Matsui J, Cameron RG, Kurian R, Kuo GC, Jeejeebhoy KN (1993) Nutritional, hepatic and me–tabolic effects of cachectin/TNF in rats receiving TPN. Gastroenterology (in press)
Mealy K, van Lanschot JJB, Robinson BG, Ramos J, Wilmore DW (1990) Are the catabolic effects of tumor necrosis factor mediated by glucocorticoids? Arch Surg 125: 42–48
Hall-Angreas M, Angreas U, Zamir O, Hasseigren P-O, Fischer JE (1990) Interaction between corticosterone and tumor necrosis factor stimulated protein breakdown in rat skeletal muscle, similar to sepsis. Surgery 108: 460–466
Moldawer LL, Svaninger G, Gelin J, Lundholm KG (1987) Interleukin-1 and tumor necrosis factor do not regulate protein balance in skeletal musele. Am J Physiol 253: C766–C773
Fraker DL, Merino MJ, Norton JA (1989) Reversal of the toxic effects of cachectin by concurrent insulin administration. Am J Physiol 256 (Endocrinol Metab 9): E725–E731
Bagby GJ, Lang CH, Skrepnik N, Spitzer JJ (1992) Attenuation of glucose metabolic changes resulting from TNF–alpha administration by adrenergic blockade. Am J Physiol 262: R628–635
Tracey KJ, Lowry SF, Beutler B, Cerami A, Albert JD, Shires GT (1986) Cachectin/tumor necrosis factor mediates changes of skeletal musele plasma membrane potential. J Exp Med 164: 1368–1373
Rennie MJ, Hundal HS, Babij P, et al. (1986) Characteristics of a glutamine carrier in skeletal musele have important consequences for nitrogen loss in injury, infection and chronic disease. Lancet 1: 1008–1012
Pichard C, Hoshino E, Allard JP, Charlton M, Atwood HL, Jeejeebhoy KN (1981) Intracellular potassium and membrane potential in rat muscles during malnutrition and subsequent refeeding. Am J Clin Nutr 54: 489–498
Pizzo SV, Gonias SL (1987) In the Receptors. Vol 1. PM Conn (ed), Academic Press Inc. Orlando FL pp 178–221
LaMarre J, Hayes MA, Wollenberg GK, Hussaini I, Hall SW, Gonias SL (1991) An alpha2-macroglobulin reeeptor-dependent mechanism for the plasma clearance of transforming growth factor-beta 1 in mice. J Clin Invest 87: 39–44
Wollenberg GK, LaMarre J, Rosendahl S, Gonias SL, Mayes MA (1991) Binding of tumor necrosis factor alpha to activated forms of human plasma alpha-2 macroglobulin. Am J Path 138: 265–272
Van Hinsberg VW, Van den Berg EA, Fiess W, Dooijewaard G (1990) Tumor necrosis factor induces the produetion of uwkinase-type Plasminogen activator by human endothelial cells. Blood 75: 1991–1998
Kristensen T, Moestrup SK, Gliemann J, Bendtsen L, Sand O, Sottrup-Jensen L (1991) Evidence that the newly cloned low-density-lipoprotein reeeptor related protein ( LRP) is the alphaimacroglobulin reeeptor. FEBS (letter) 276: 151–155
Goldberg AL (1979) Influence of insulin and contraetile activity on musele size and protein balance. Diabetes 28 (suppl 1): 18–24
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Jeejeebhoy, K.N. (1993). Interaction of Tumor Necrosis Factor/ Cachectin and Nutrition. In: Vincent, JL. (eds) Yearbook of Intensive Care and Emergency Medicine 1993. Yearbook of Intensive Care and Emergency Medicine 1993, vol 1993. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-84904-6_19
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DOI: https://doi.org/10.1007/978-3-642-84904-6_19
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