Die metabolische Selbstzerstörung des kritisch kranken Patienten (Teil I): Evolutionsbiologische Hintergründe, Mechanismen und Sinnhaftigkeit^{[1] [2]}

Zusammenfassung

Die Übersicht möchte potenziell selbstzerstörerische metabolische Reaktionen, die man häufig bei kritisch kranken Patienten beobachten kann, aus evolutionsbiologischer Sicht betrachten, und dabei in einem 1. Teil auf deren Ursprung, Mechanismen und Sinnhaftigkeit genauer eingehen. Metabolische Reaktionen, die besonders nach chirurgischer Homöostasestörung (Trauma, Sepsis) regelhaft auftreten, umfassen die Hyperglykämie, die Insulinresistenz, eine erhöhte hepatische Glukoseproduktion und einen gesteigerten muskulären Eiweißabbau. Aus evolutionsbiologischer Sicht waren diese metabolischen Sekundärreaktionen notwendig und auch erfolgreich. Nur dadurch konnte im Rahmen der Phylogenese die Wahrscheinlichkeit erhöht werden, leichtere chirurgische Traumata auch ohne fremde Hilfe (spontan) überleben zu können. Teleologisch stand dabei die Gewährleistung zellulärer Funktionen, die für Infektabwehr und Gewebereparatur unerlässlich sind, im Vordergrund. Aufgrund unvermeidbarer evolutionsbiologischer Zwänge haben diese metabolischen Sekundärreaktionen bis in die Neuzeit hinein überlebt.

Abstract

The present study wants to analyse potentially self-destructive metabolic responses observed in critically ill patients from an evolutionary perspective specifically focusing on origins, nature, and principal usefulness. Metabolic reactions associated with surgical injury or infection comprise hyperglycemia, insulin resistance, increased hepatic glucose production and muscle protein breakdown. From an evolutionary perspective these responses have been necessary and successful to overcome spontaneously survivable insults (minor surgical trauma) by maintaining function of immune-competent and reparative cells. There is, however, overwhelming evidence that extreme metabolic responses have not been selected by evolution, but may have persisted because of unavoidable evolutionary constraints.

Schlüsselwörter

Autokannibalismus - schwere Sepsis - Trauma - Schock - Phylogenese - Evolution - Hyperglykämie - Kohlenhydratstoffwechsel - Proteinstoffwechsel - adaptive Reaktion

Keywords

auto-cannibalism - severe sepsis - trauma - shock - phylogenesis - evolution - hyperglycemia - carbohydrate metabolism - protein metabolism - adaptive response

¹ Im Original publiziert unter: Hartl WH, Jauch KW. Metabolic self-destruction in critically ill patients: Origins, mechanisms and therapeutic principles. Nutrition 2014 Mar; 30 (3): 261 – 267

² Nachdruck aus: DIVI Journal 2015; 6: 96 – 101

• Literatur

• 1 Waterlow JC. The nature and significance of nutritional adaptation. Eur J Clin Nutr 1999; 53 (Suppl. 01) S2-5
• 2 Corathers SD, Falciglia M. The role of hyperglycemia in acute illness: supporting evidence and its limitations. Nutrition 2011; 27: 276-281
• 3 Englesbe MJ, Patel SP, He K et al. Sarcopenia and mortality after liver transplantation. J Am Coll Surg 2010; 211: 271-278
• 4 Norman K, Pichard C, Lochs H et al. Prognostic impact of disease-related malnutrition. Clin Nutr 2008; 27: 5-15
• 5 Gruther W, Benesch T, Zorn C et al. Muscle wasting in intensive care patients: ultrasound observation of the M. quadriceps femoris muscle layer. J Rehabil Med 2008; 40: 185-189
• 6 Plank LD, Hill GL. Similarity of changes in body composition in intensive care patients following severe sepsis or major blunt injury. Ann N Y Acad Sci 2000; 904: 592-602
• 7 Cerra FB, Siegel JH, Coleman B et al. Septic autocannibalism. A failure of exogenous nutritional support. Ann Surg 1980; 192: 570-580
• 8 Weil ZM, Norman GJ, DeVries AC et al. The injured nervous system: a Darwinian perspective. Prog Neurobiol 2008; 86: 48-59
• 9 Hardaway RM. Wound shock: a history of its study and treatment by military surgeons. Mil Med 2004; 169: 265-269
• 10 Trunkey DD. History and development of trauma care in the United States. Clin Orthop Relat Res 2000; 374: 36-46
• 11 Odero W, Khayesi M, Heda PM. Road traffic injuries in Kenya: magnitude, causes and status of intervention. Inj Control Saf Promot 2003; 10: 53-61
• 12 Griffiths J, Waldmann C, Quinlan J. Sexual dysfunction in intensive care survivors. Br J Hosp Med (Lond) 2007; 68: 470-473
• 13 Holliday R. Evolution of human longevity, population pressure and the origins of warfare. Biogerontology 2005; 6: 363-368
• 14 Meindl R. Human populations before agriculture. In: Jones S, Martin R, Pilbeam D, eds. The Cambridge Encyclopedia of Human Evolution. Cambridge: Cambridge University Press; 1992: 406-410
• 15 Finch CE. Evolution in health and medicine Sackler colloquium: Evolution of the human lifespan and diseases of aging: roles of infection, inflammation, and nutrition. Proc Natl Acad Sci U S A 2010; 107 (Suppl. 01) 1718-1724
• 16 Keppie NJ, Naylor JM. A retrospective study of the diagnoses and survival of elk admitted to a large animal referral clinic. Can Vet J 2005; 46: 325-330
• 17 Scott M. Musculoskeletal injuries in nonracing quarter horses. Vet Clin North Am Equine Pract 2008; 24: 133-152
• 18 Ottaviani E, Franceschi C. The invertebrate phagocytic immunocyte: clues to a common evolution of immune and neuroendocrine systems. Immunol Today 1997; 18: 169-174
• 19 Scapigliati G. Models and evolution of inflammatory activities. Curr Pharm Des 2010; 16: 4159
• 20 Kaiser P, Rothwell L, Avery S et al. Evolution of the interleukins. Dev Comp Immunol 2004; 28: 375-394
• 21 Ottaviani E. Evolution of immune-neuroendocrine integration from an ecological immunology perspective. Cell Tissue Res 2011; 344: 213-215
• 22 Denver RJ. Structural and functional evolution of vertebrate neuroendocrine stress systems. Ann N Y Acad Sci 2009; 1163: 1-16
• 23 Andersson U, Tracey KJ. Neural reflexes in inflammation and immunity. J Exp Med 2012; 209: 1057-1068
• 24 Hotamisligil GS. Inflammation and metabolic disorders. Nature 2006; 444: 860-867
• 25 Soeters MR, Soeters PB. The evolutionary benefit of insulin resistance. Clin Nutr 2012; 31: 1002-1007
• 26 Waterlow JC. Protein-energy malnutrition: Challenges and controversies. Proc Nutr Soc India 1991; 37: 59-86
• 27 Reeds PJ, Jahoor F. The amino acid requirements of disease. Clin Nutr 2001; 20 (Suppl. 01) 15-22
• 28 Marimuthu K, Murton AJ, Greenhaff PL. Mechanisms regulating muscle mass during disuse atrophy and rehabilitation in humans. J Appl Physiol 2011; 110: 555-560
• 29 Ferrando AA, Wolfe RR. Restoration of hormonal action and muscle protein. Crit Care Med 2007; 35 (Suppl. 09) S630-634
• 30 Fanzani A, Conraads VM, Penna F et al. Molecular and cellular mechanisms of skeletal muscle atrophy: an update. J Cachexia Sarcopenia Muscle 2012; 3: 163-179
• 31 Li P, Yin YL, Li D et al. Amino acids and immune function. Br J Nutr 2007; 98: 237-252
• 32 Calder PC, Dimitriadis G, Newsholme P. Glucose metabolism in lymphoid and inflammatory cells and tissues. Curr Opin Clin Nutr Metab Care 2007; 10: 531-540
• 33 MacIver NJ, Jacobs SR, Wieman HL et al. Glucose metabolism in lymphocytes is a regulated process with significant effects on immune cell function and survival. J Leukoc Biol 2008; 84: 949-957
• 34 Maggs DG, Jacob R, Rife F et al. Interstitial fluid concentrations of glycerol, glucose, and amino acids in human quadriceps muscle and adipose tissue. Evidence for significant lipolysis in skeletal muscle. J Clin Invest 1995; 96: 370-377
• 35 Maclean DA, Bangsbo J, Saltin B. Muscle interstitial glucose and lactate levels during dynamic exercise in humans determined by microdialysis. J Appl Physiol 1999; 87: 1483-1490
• 36 Ljungqvist O, Jansson E, Ware J. Effect of food deprivation on survival after hemorrhage in the rat. Circ Shock 1987; 22: 251-260
• 37 Mizock BA. Alterations in fuel metabolism in critical illness: hyperglycaemia. Best Pract Res Clin Endocrinol Metab 2001; 15: 533-551
• 38 Dungan KM, Braithwaite SS, Preiser JC. Stress hyperglycaemia. Lancet 2009; 373: 1798-1807
• 39 Gerich JE. Control of glycaemia. Baillieres Clin Endocrinol Metab 1993; 7: 551-586
• 40 McGuinness OP. Defective glucose homeostasis during infection. Annu Rev Nutr 2005; 25: 9-35
• 41 Dahn MS, Mitchell RA, Lange MP et al. Hepatic metabolic response to injury and sepsis. Surgery 1995; 117: 520-530
• 42 Wahren J, Ekberg K. Splanchnic regulation of glucose production. Annu Rev Nutr 2007; 27: 329-345
• 43 Long CL, Nelson KM. Nutritional requirements based on substrate fluxes in trauma. Nutr Res 1993; 13: 1459-1478
• 44 Mészáros K, Lang CH, Bagby GJ et al. In vivo glucose utilization by individual tissues during nonlethal hypermetabolic sepsis. FASEB J 1988; 2: 3083-3086
• 45 Spolarics Z, Schuler A, Bagby GJ et al. Tumor necrosis factor increases in vivo glucose uptake in hepatic nonparenchymal cells. J Leukoc Biol 1991; 49: 309-312