Abnormalities in glucose metabolism and their relevance to nutrition support in the critically ill

Current Opinion in Clinical Nutrition and Metabolic Care

Volumn 1, Issue 2, 1998, Pages 191-194

  Webber, Jonathan ^a  

^a SELLY OAK HOSPITAL   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

CYTOKINE; GLUCOSE; HORMONE;

ANIMAL; CRITICAL ILLNESS; HUMAN; INSULIN RESISTANCE; METABOLISM; NUTRITIONAL STATUS; NUTRITIONAL SUPPORT; PHYSIOLOGY; REVIEW;

ANIMALS; CRITICAL ILLNESS; CYTOKINES; GLUCOSE; HORMONES; HUMANS; INSULIN RESISTANCE; NUTRITIONAL STATUS; NUTRITIONAL SUPPORT;

EID: 0032009789     PISSN: 13631950     EISSN: None     Source Type: Journal    
DOI: 10.1097/00075197-199803000-00009     Document Type: Article

References (35)

1. Mizock BA. Alterations in carbohydrate metabolism during stress: a review of the literature. Am J Med 1995; 98:75-84.
2. Shaw JHF, Wolfe RR. Energy and protein metabolism in sepsis and trauma. Aust N Z J Surg 1987; 57:41-47.
3. Shangraw RE, Jahoor F, Miyoshi H, Neff WA, Stuart CA, Herndon DA, Wolfe RR. Differentiation between septic and postburn insulin resistance. Metabolism 1989; 38:983-989.
4. McGuiness OP, Shau V, Benson EM, Lewis M, Snowden RT, Greene JE, et al. Role of epinephrine and norepinephrine in the metabolic response to stress hormone infusion in the conscious dog. Am J Physiol 1997; 273:E674-E681.
5. Chu CA, Sindelar DK, Neal DW, Allen EJ, Donahue EP, Cherrington AD. Comparison of the direct and indirect effects of epinephrine on hepatic glucose production. J Clin Invest 1997; 99:1044-1056.
6. Stumvoll M, Meyer C, Mitrakou A, Nadkarni V, Gerich JE. Renal glucose production and utilization: new aspects in humans. Diabetologia 1997; 40:749-757.
7. Maitra SR, Homan CS, Pan W, Geller ER, Henry MC, Thode HC Jr. Renal gluconeogenesis and blood flow during endotoxic shock. Acad Emerg Med 1996; 3:1006-1010.
8. Dahn MS, Mitchell RA, Lange MP, Smith S, Jacobs LA. Hepatic metabolic response to injury and sepsis. Surgery 1995; 117:520-530.
9. Lang CH, Cooney R, Vary TC. Central interleukin-1 partially mediates endotoxin-induced changes in glucose metabolism. Am J Physiol 1996; 271:E309-E316. Using an IL-1 receptor antagonist administered centrally, this study shows that many of the effects of endotoxin on glucose metabolism can be blocked.
10. Sakurai Y, Zhang X-J, Wolfe RR. Short-term effects of tumor necrosis factor on substrate and energy metabolism in dogs. J Clin Invest 1993; 91:2437-2445.
11. Sakurai Y, Zhang X-J, Wolfe RR. TNF directly stimulates glucose uptake and leucine oxidation and inhibits FFA flux in conscious dogs. Am J Physiol 1996; 270:E864-E872. By employing a pancreatic clamp technique, this study demonstrates that TNF itself does not augment endogenous glucose production, but that this is a glucagon effect. TNF lowers blood glucose by stimulating non-insulin-mediated glucose uptake.
12. Metzger S, Begleibter N, Barash V, Drize O, Peretz T, Shiloni E, Chajek-Shaul T. Tumor necrosis factor inhibits the transcriptional rate of glucose-6-phosphatase in vivo and in vitro. Metabolism 1997; 46:579-583.
13. Chang CK, Gatan M, Schumer W. Efficacy of anti-tumor necrosis factor polyclonal antibody on phosphoenolpyruvate carboxykinase expression in septic and endotoxemic rats. Shock 1996; 6:57-60.
14. Long CL, Nelson KM, Geiger JW, Theus WL, Clark JA, Laws HL, Blakemore WS. Effect of amino acid infusion on glucose production in trauma patients. J Trauma 1996; 40:335-341.
15. Jahoor F, Peters EJ, Wolfe RR. The relationship between gluconeogenio substrate supply and glucose production in humans. Am J Physiol 1990; 258:E288-E296.
16. Watters JM, Norris SB, Kirkpatrick SM. Endogenous glucose production following injury increases with age. J Clin Endocrin Metab 1997; 82:3005-3010.
17. Gore DC, Jahoor F, Hibbert JM, DeMaria EJ. Lactic acidosis during sepsis is related to increased pyruvate production, not deficits in tissue oxygen availability. Ann Surg 1996; 224:97-102. This study in severely septic patients demonstrates that hyperlactinaemia is due to increased flux through the glycolytic pathway and not the result of hypoxia.
18. James JH, Fang CH, Schrantz SJ, Hasselgren PO, Paul RJ, Fischer JE. Linkage of aerobic glycolysis to sodium-potassium transport in rat skeletal muscle. Implications for increased muscle lactate production in sepsis. J Clin Invest 1996; 98:2388-2397.
19. Carter EA, Tompkins RG, Babich JW, Correia J, Bailey EM, Fischman AJ. Thermal injury in rats alters glucose utilization by skin, wound, and small intestine, but not by skeletal muscle. Metabolism 1996; 45:1161-1167. This study shows that enhanced glucose utilization after burn injury in rats occurs primarily in the wound area and is associated with increased hexokinase activity.
20. Thorell A, Loftenius A, Andersson B, Ljungqvist O. Postoperative insulin resistance and circulating concentrations of stress hormones and cytokines. Clin Nutr 1996; 15:75-79.
21. Kotani G, Usami M, Kasahara H, Saitoh Y. The relationship of IL-6 to hormonal mediators, fuel utilization and systemic hypermetabolism after surgical trauma. Kobe J Med Sci 1996; 42:187-205.
22. Lang CH, Dobbrescu C, Bagby GJ. Tumor necrosis factor impairs insulin action on peripheral glucose disposal and hepatic glucose output. Endocrinology 1992; 130:43-52.
23. Ling PR, Bistrian BR, Mendez B, Istfan NW. Effects of systemic infusions of endotoxin, tumor necrosis factor and interleukin-1 on glucose metabolism in the rat: relationship to endogenous glucose production and peripheral glucose tissue uptake. Metabolism 1994; 43:279-284.
24. Miles PDG, Romeo OM, Higo K, Cohen A, Rafaat K, Olefsky JM. TNF-α-induced insulin resistance in vivo and its prevention by troglitazone. Diabetes 1997; 46:1678-1683.
25. Fan J, Li YH, Wojnar MM, Lang CH. Endotoxin-induced alterations in insulin-stimulated phosphorylation of insulin receptor, IRS-1, and MAP kinase in skeletal muscle. Shock 1996; 6:164-170.
26. Vary TC. Sepsis-induced alterations in pyruvate dehydrogenase complex activity in rat skeletal muscle: effects on plasma lactate. Shock 1996; 6:89-94.
27. Gore DC, Jahoor F, Hibbert J, DeMaria EJ. Except for alanine, muscle protein catabolism is not influenced by alterations in glucose metabolism during sepsis. Arch Surg 1995; 130:1171-1177.
28. Shangraw RE, Jahoor F, Wolfe RR, Lang CH. Pyruvate dehydrogenase inactivity is not responsible for sepsis-induced insulin resistance. Crit Care Med 1996; 24:566-574. In studies in septic patients and in rats the authors clearly show that activation of PDH with dichloroacetate does not reverse whole-body or skeletal muscle insulin-mediated glucose uptake. However, the impairment seen in cardiac muscle was reversed and this may be of clinical relevance because myocardial contractility is reduced in sepsis.
29. Askanazi J, Carpentier YA, Elwyn DH, Nordenstrom J, Jeevanandam M, Rosenbaum SH, et al. Influence of total parenteral nutrition on fuel utilization in injury and sepsis. Ann Surg 1980; 191:40-46.
30. Shaw JHF, Wolfe RR. An integrated analysis of glucose, fat, and protein metabolism in severely traumatized patients. Ann Surg 1989; 209:63-72.
31. Jeevanandam M, Holaday NJ, Petersen SR. Adjuvant recombinant human growth hormone does not augment endogenous glucose production in total parenteral nutrition fed multiple trauma patients. Metabolism 1996; 45:450-456.
32. Crown AL, Holly JMP. The insulin-like growth factor system in critical illness: pathophysiology and therapeutic potential. Clin Nutr 1995; 14:321-328.
33. Wolf SE, Barrow RE, Herndon DN. Growth hormone and 1GF-1 therapy in the hypercatabolic patient. Baillieres Clin Endocrinol Metab 1996; 10:447-463.
34. Ling PR, Sierra P, Qu Z, Bistrian BR. Insulin-like growth factor-1 improves glucose utilization in tumour necrosis factor-treated rats under hyperinsulinemic euglycemic conditions. Metabolism 1997; 46:1052-1058. In TNF-treated rats IGF-1 increases muscle glucose disposal. The authors suggest that this effect may be mediated by IGF-1 receptors, or may be an effect of IGF-1 downstream of the insulin receptor.
35. Lang CH. IGF-1 stimulates muscle glucose uptake during sepsis. Shock 1996; 5:22-27.