Stress-hyperglycemia, insulin and immunomodulation in sepsis
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[1] M. Papa,et al. Tumor necrosis factor alpha-induced phosphorylation of insulin receptor substrate-1 (IRS-1). Possible mechanism for suppression of insulin-stimulated tyrosine phosphorylation of IRS-1. , 1995, The Journal of biological chemistry.
[2] R. Natarajan,et al. Molecular Mechanisms of Tumor Necrosis Factor α Gene Expression in Monocytic Cells via Hyperglycemia-induced Oxidant Stress-dependent and -independent Pathways* , 2000, The Journal of Biological Chemistry.
[3] M. Karin,et al. Nuclear factor-kappaB: a pivotal transcription factor in chronic inflammatory diseases. , 1997, The New England journal of medicine.
[4] J H Siegel,et al. Physiological and metabolic correlations in human sepsis. Invited commentary. , 1979, Surgery.
[5] P. Pozzilli,et al. Infections and Diabetes: Mechanisms and Prospects for Prevention , 1994, Diabetic medicine : a journal of the British Diabetic Association.
[6] Barry A. Mizoch. Alterations in Fuel Metabolism in Critical Illness , 1997 .
[7] S. Baldwin,et al. Interleukin 1 stimulates hexose transport in fibroblasts by increasing the expression of glucose transporters. , 1990, The Journal of biological chemistry.
[8] R. Wolfe. Substrate utilization/insulin resistance in sepsis/trauma. , 1997, Bailliere's clinical endocrinology and metabolism.
[9] A. Imrich,et al. Immunologic effects of acute hyperglycemia in nondiabetic rats. , 1997, JPEN. Journal of parenteral and enteral nutrition.
[10] A. Ceriello,et al. Meal-induced oxidative stress and low-density lipoprotein oxidation in diabetes: the possible role of hyperglycemia. , 1999, Metabolism: clinical and experimental.
[11] G. Van den Berghe,et al. Regulation of insulin-like growth factor binding protein-1 during protracted critical illness. , 2002, The Journal of clinical endocrinology and metabolism.
[12] D. Benos,et al. Localization of amiloride-sensitive sodium channels in A6 cells by atomic force microscopy. , 1997, The American journal of physiology.
[13] K. Malmberg. Prospective randomised study of intensive insulin treatment on long term survival after acute myocardial infarction in patients with diabetes mellitus , 1997, BMJ.
[14] K. Anderson,et al. A conserved signaling pathway: the Drosophila toll-dorsal pathway. , 1996, Annual review of cell and developmental biology.
[15] J. Spitzer,et al. Tumor necrosis factor increases in vivo glucose utilization of macrophage-rich tissues. , 1987, Biochemical and biophysical research communications.
[16] J. Chiasson,et al. Inhibitory effect of epinephrine on insulin-stimulated glucose uptake by rat skeletal muscle. , 1981, The Journal of clinical investigation.
[17] S. Akira,et al. Cutting edge: Toll-like receptor 4 (TLR4)-deficient mice are hyporesponsive to lipopolysaccharide: evidence for TLR4 as the Lps gene product. , 1999, Journal of immunology.
[18] T. Evans. Hemodynamic and metabolic therapy in critically ill patients. , 2001, The New England journal of medicine.
[19] L. Rydén,et al. Admission plasma glucose. Independent risk factor for long-term prognosis after myocardial infarction even in nondiabetic patients. , 1999, Diabetes care.
[20] B. Spiegelman,et al. IRS-1-Mediated Inhibition of Insulin Receptor Tyrosine Kinase Activity in TNF-α- and Obesity-Induced Insulin Resistance , 1996, Science.
[21] D. Mannino,et al. The epidemiology of sepsis in the United States from 1979 through 2000. , 2003, The New England journal of medicine.
[22] K. Zibara,et al. Acute Hyperglycaemia Induces Changes in the Transcription Levels of 4 Major Genes in Human Endothelial Cells: Macroarrays-based Expression Analysis , 2002, Thrombosis and Haemostasis.
[23] A. Malhotra,et al. Stress-induced hyperglycemia. , 2001, Critical care clinics.
[24] P. Marik,et al. Gastric versus post-pyloric feeding: a systematic review , 2003, Critical care.
[25] N. Webster,et al. Increased nuclear factor κB activation in critically ill patients who die , 2000 .
[26] R. Bone,et al. Sir Isaac Newton, sepsis, SIRS, and CARS. , 1996, Critical care medicine.
[27] R. Bone,et al. Sepsis: a new hypothesis for pathogenesis of the disease process. , 1997, Chest.
[28] G. Grunkemeier,et al. Continuous intravenous insulin infusion reduces the incidence of deep sternal wound infection in diabetic patients after cardiac surgical procedures. , 1999, The Annals of thoracic surgery.
[29] J Herlitz,et al. Randomized trial of insulin-glucose infusion followed by subcutaneous insulin treatment in diabetic patients with acute myocardial infarction (DIGAMI study): effects on mortality at 1 year. , 1995, Journal of the American College of Cardiology.
[30] R. Marfella,et al. Vascular effects of acute hyperglycemia in humans are reversed by L-arginine. Evidence for reduced availability of nitric oxide during hyperglycemia. , 1997, Circulation.
[31] B. B. Hart,et al. Catecholamines: study of interspecies variation. , 1989, Critical care medicine.
[32] C. Hack,et al. Role of cytokines in sepsis. , 1997, Advances in immunology.
[33] S. Kawachi,et al. Role of nitric oxide in the regulation of acute and chronic inflammation. , 2000, Antioxidants & redox signaling.
[34] C. Natanson,et al. The sirens' songs of confirmatory sepsis trials: selection bias and sampling error. , 1998, Critical Care Medicine.
[35] P. Marik,et al. Adrenal insufficiency in the critically ill: a new look at an old problem. , 2002, Chest.
[36] Jianping Ye,et al. Serine Phosphorylation of Insulin Receptor Substrate 1 by Inhibitor κB Kinase Complex* 210 , 2002, The Journal of Biological Chemistry.
[37] P. Marik,et al. Early enteral nutrition in acutely ill patients: A systematic review , 2001, Critical care medicine.
[38] J. Liao,et al. Inducible nitric oxide: an autoregulatory feedback inhibitor of vascular inflammation. , 1998, Journal of immunology.
[39] C. Sprung,et al. The ACCP-SCCM consensus conference on sepsis and organ failure. , 1992, Chest.
[40] Miet Schetz,et al. Outcome benefit of intensive insulin therapy in the critically ill: Insulin dose versus glycemic control* , 2003, Critical care medicine.
[41] J. Dunlap,et al. Effect of increased concentration of D-glucose or L-fucose on monocyte adhesion to endothelial cell monolayers and activation of nuclear factor-kappaB. , 2002, Metabolism: clinical and experimental.
[42] Charles Natanson,et al. Risk and the efficacy of antiinflammatory agents: retrospective and confirmatory studies of sepsis. , 2002, American journal of respiratory and critical care medicine.
[43] C. Lang,et al. Gram-negative infection increases noninsulin-mediated glucose disposal. , 1991, Endocrinology.
[44] M. Jeevanandam,et al. Glucose turnover, oxidation, and indices of recycling in severely traumatized patients. , 1990, The Journal of trauma.
[45] P. Marik,et al. Death by parenteral nutrition , 2003, Intensive Care Medicine.
[46] G. Clermont,et al. Epidemiology of severe sepsis in the United States: Analysis of incidence, outcome, and associated costs of care , 2001, Critical care medicine.
[47] K. Taylor,et al. Admission plasma glucose: an independent risk factor in nondiabetic women after coronary artery bypass grafting. , 2001, Diabetes care.
[48] A. Aljada,et al. Insulin inhibits the pro-inflammatory transcription factor early growth response gene-1 (Egr)-1 expression in mononuclear cells (MNC) and reduces plasma tissue factor (TF) and plasminogen activator inhibitor-1 (PAI-1) concentrations. , 2002, The Journal of clinical endocrinology and metabolism.
[49] I. Macdonald,et al. Septic patients in multiple organ failure can oxidize infused glucose, but non-oxidative disposal (storage) is impaired. , 1995, Clinical science.
[50] G. Grunkemeier,et al. Glucose control lowers the risk of wound infection in diabetics after open heart operations. , 1997, The Annals of thoracic surgery.
[51] P. Kuo,et al. Endotoxin-mediated S-nitrosylation of p50 alters NF-kappa B-dependent gene transcription in ANA-1 murine macrophages. , 1999, Journal of immunology.
[52] H. Gerstein,et al. Stress Hyperglycemia and Prognosis of Stroke in Nondiabetic and Diabetic Patients: A Systematic Overview , 2001, Stroke.
[53] L. Khaodhiar,et al. Perioperative hyperglycemia, infection or risk? , 1999, Current opinion in clinical nutrition and metabolic care.
[54] B. Kahn,et al. Glucose transporters and insulin action--implications for insulin resistance and diabetes mellitus. , 1999, The New England journal of medicine.
[55] J. Vincent,et al. Has the mortality of septic shock changed with time. , 1998, Critical care medicine.
[56] A. Aljada,et al. Nuclear factor-kappaB suppressive and inhibitor-kappaB stimulatory effects of troglitazone in obese patients with type 2 diabetes: evidence of an antiinflammatory action? , 2001, The Journal of clinical endocrinology and metabolism.
[57] C. Lang,et al. Tumor necrosis factor mediates zymosan-induced increase in glucose flux and insulin resistance. , 1995, The American journal of physiology.
[58] B. Obermaier,et al. Decreased tyrosine kinase activity of insulin receptor isolated from rat adipocytes rendered insulin-resistant by catecholamine treatment in vitro. , 1986, The Biochemical journal.
[59] C. Lang,et al. Sepsis-induced insulin resistance in rats is mediated by a beta-adrenergic mechanism. , 1992, The American journal of physiology.
[60] H Wedel,et al. Infarction : Long-Term Results From the Diabetes and Insulin-Glucose Infusion Conventionally Treated Patients With Diabetes Mellitus and Acute Myocardial Glycometabolic State at Admission : Important Risk Marker of Mortality in , 1999 .
[61] D. Männel,et al. Role of NFkappaB in the mortality of sepsis. , 1997, The Journal of clinical investigation.
[62] D. Herndon,et al. The Effects of Hyperglycemia on Skin Graft Survival in the Burn Patient , 2000, Annals of plastic surgery.
[63] J. Renart,et al. Predictive Value of Nuclear Factor κB Activity and Plasma Cytokine Levels in Patients with Sepsis , 2000, Infection and Immunity.
[64] G. Van den Berghe,et al. Intensive insulin therapy exerts antiinflammatory effects in critically ill patients and counteracts the adverse effect of low mannose-binding lectin levels. , 2003, The Journal of clinical endocrinology and metabolism.
[65] J. S. Elmendorf,et al. Growth hormone-induced insulin resistance: role of the insulin receptor, IRS-1, GLUT-1, and GLUT-4. , 1997, The American journal of physiology.
[66] M. Fink. Nuclear factor-κB: Is it a therapeutic target for the adjuvant treatment of sepsis? , 2003 .
[67] P. Marik. Nuclear factor-κb inhibition in sepsis: Steroids versus specific nuclear factor-κb inhibitors? * , 2002 .
[68] Cerra Fb,et al. Hypermetabolism, organ failure, and metabolic support. , 1987 .
[69] T. Standiford,et al. Expression and regulation of chemokines in bacterial pneumonia , 1996, Journal of leukocyte biology.
[70] P. Taccone,et al. Sepsis: state of the art. , 2003, Minerva anestesiologica.
[71] M. Laville,et al. Insulin sensitivity of glucose and fat metabolism in severe sepsis. , 2000, Clinical science.
[72] A. Saltiel,et al. Signaling pathways in insulin action: molecular targets of insulin resistance. , 2000, The Journal of clinical investigation.
[73] L. Moldawer,et al. Stimulatory effect of interleukin-1 upon hepatic metabolism. , 1986, Metabolism: clinical and experimental.
[74] A. Ceriello,et al. Coagulation activation in diabetes mellitus: the role of hyperglycaemia and therapeutic prospects , 1993, Diabetologia.
[75] J. Palmer,et al. Low-dose interleukin 1 and tumor necrosis factor individually stimulate insulin release but in combination cause suppression. , 1994, European journal of endocrinology.
[76] W. Bao,et al. In Vivo Myocardial Protection From Ischemia/Reperfusion Injury by the Peroxisome Proliferator–Activated Receptor-&ggr; Agonist Rosiglitazone , 2001, Circulation.
[77] M. Lange,et al. The relationship of insulin production to glucose metabolism in severe sepsis. , 1985, Archives of surgery.
[78] E. Hirsch,et al. Blood insulin responses to blood glucose levels in high output sepsis and spetic shock. , 1978, American journal of surgery.
[79] F. Cerra,et al. Hypermetabolism, organ failure, and metabolic support. , 1987, Surgery.
[80] H. Bingham,et al. Physiological and metabolic correlations in human sepsis , 1980 .
[81] G. Dimitriadis,et al. Effects of glucocorticoid excess on the sensitivity of glucose transport and metabolism to insulin in rat skeletal muscle. , 1997, The Biochemical journal.
[82] L. McManus,et al. Agonist‐dependent failure of neutrophil function in diabetes correlates with extent of hyperglycemia , 2001, Journal of leukocyte biology.
[83] N. Gay,et al. Drosophila Toll and IL-1 receptor , 1991, Nature.
[84] K. P. Ober. Endocrinology of Critical Disease , 1997, Contemporary Endocrinology.
[85] B A Mizock,et al. Alterations in fuel metabolism in critical illness: hyperglycaemia. , 2001, Best practice & research. Clinical endocrinology & metabolism.
[86] A. Malik,et al. Inhibition of NF-kappaB activation by pyrrolidine dithiocarbamate prevents In vivo expression of proinflammatory genes. , 1999, Circulation.
[87] Nielson Cp,et al. Inhibition of Polymorphonuclear Leukocyte Respiratory Burst by Elevated Glucose Concentrations in Vitro , 1989 .
[88] A. Aljada,et al. Effect of insulin on human aortic endothelial nitric oxide synthase. , 2000, Metabolism: clinical and experimental.
[89] A. Gelb,et al. Propofol Anesthesia Compared to Awake Reduces Infarct Size in Rats , 2002, Anesthesiology.
[90] I. Kowalska,et al. Plasma interleukin-8 concentrations are increased in obese subjects and related to fat mass and tumor necrosis factor-alpha system. , 2002, The Journal of clinical endocrinology and metabolism.
[91] B. Spiegelman,et al. Reduced tyrosine kinase activity of the insulin receptor in obesity-diabetes. Central role of tumor necrosis factor-alpha. , 1994, The Journal of clinical investigation.
[92] A. Aljada,et al. Glucose challenge stimulates reactive oxygen species (ROS) generation by leucocytes. , 2000, The Journal of clinical endocrinology and metabolism.
[93] F. Dominici,et al. Alterations in the early steps of the insulin-signaling system in skeletal muscle of GH-transgenic mice. , 1999, The American journal of physiology.
[94] Jianping Ye,et al. Serine phosphorylation of insulin receptor substrate 1 by inhibitor kappa B kinase complex. , 2002, The Journal of biological chemistry.
[95] R. Little,et al. Insulin resistance and substrate utilization in human endotoxemia. , 2000, The Journal of clinical endocrinology and metabolism.
[96] N. Webster,et al. Increased nuclear factor kappa B activation in critically ill patients who die. , 2000, Critical care medicine.
[97] A. Aljada,et al. Insulin inhibits intranuclear nuclear factor kappaB and stimulates IkappaB in mononuclear cells in obese subjects: evidence for an anti-inflammatory effect? , 2001, The Journal of clinical endocrinology and metabolism.
[98] B. Spiegelman,et al. Tumor necrosis factor alpha inhibits signaling from the insulin receptor. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[99] R. McIntyre,et al. L-arginine decreases alveolar macrophage proinflammatory monokine production during acute lung injury by a nitric oxide synthase-dependent mechanism. , 1997, The Journal of trauma.
[100] J. Woo,et al. The influence of hyperglycemia and diabetes mellitus on immediate and 3-month morbidity and mortality after acute stroke. , 1990, Archives of neurology.
[101] Y. Higashimoto,et al. Modulation of proinflammatory cytokines by nitric oxide in murine acute lung injury. , 1999, American journal of respiratory and critical care medicine.
[102] J. Liao,et al. Inhibition of Endothelial Vascular Cell Adhesion Molecule-1 Expression by Nitric Oxide Involves the Induction and Nuclear Translocation of IκBα* , 1997, The Journal of Biological Chemistry.
[103] A. Aljada,et al. Tumor necrosis factor-alpha inhibits insulin-induced increase in endothelial nitric oxide synthase and reduces insulin receptor content and phosphorylation in human aortic endothelial cells. , 2002, Metabolism: clinical and experimental.
[104] A. Aljada,et al. The potential therapeutic role of insulin in acute myocardial infarction in patients admitted to intensive care and in those with unspecified hyperglycemia. , 2003, Diabetes care.
[105] J. Carvalheira,et al. Tissue-specific regulation of early steps in insulin action in septic rats. , 2001, Life sciences.
[106] R. Little,et al. Selective impairment of glucose storage in human sepsis , 1999, The British journal of surgery.
[107] D. Frankenfield,et al. Correlation between measured energy expenditure and clinically obtained variables in trauma and sepsis patients. , 1994, JPEN. Journal of parenteral and enteral nutrition.
[108] J. Christman,et al. Nuclear factor k B: a pivotal role in the systemic inflammatory response syndrome and new target for therapy , 1998, Intensive Care Medicine.
[109] M. Beach,et al. Insulin infusion improves neutrophil function in diabetic cardiac surgery patients. , 1999, Anesthesia and analgesia.
[110] S. Cuzzocrea,et al. Ligands of the peroxisome proliferator‐activated receptors (PPAR‐γ and PPAR‐α) reduce myocardial infarct size , 2002, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[111] R. Wolfe,et al. TNF directly stimulates glucose uptake and leucine oxidation and inhibits FFA flux in conscious dogs. , 1996, The American journal of physiology.
[112] K. Patrick Ober,et al. Alterations in Fuel Metabolism in Critical Illness , 1997 .
[113] H. Pahl,et al. Activators and target genes of Rel/NF-kappaB transcription factors. , 1999, Oncogene.
[114] D. Leroith,et al. A molecular basis for insulin resistance. Elevated serine/threonine phosphorylation of IRS-1 and IRS-2 inhibits their binding to the juxtamembrane region of the insulin receptor and impairs their ability to undergo insulin-induced tyrosine phosphorylation. , 2009, The Journal of biological chemistry.
[115] C. Nelson,et al. Inhibition of Polymorphonuclear Leukocyte Respiratory Burst by Elevated Glucose Concentrations in Vitro , 1989, Diabetes.
[116] G. Berghe. Neuroendocrine pathobiology of chronic critical illness. , 2002 .
[117] A. Aljada,et al. Nuclear Factor-κB Suppressive and Inhibitor-κB Stimulatory Effects of Troglitazone in Obese Patients with Type 2 Diabetes: Evidence of an Antiinflammatory Action?1 , 2001 .
[118] A. Aljada,et al. Suppression of nuclear factor-kappaB and stimulation of inhibitor kappaB by troglitazone: evidence for an anti-inflammatory effect and a potential antiatherosclerotic effect in the obese. , 2001, The Journal of clinical endocrinology and metabolism.
[119] B. Bistrian,et al. Intensive insulin therapy in critically ill patients. , 2002, The New England journal of medicine.
[120] J. Liao,et al. Differential regulation of endothelial cell adhesion molecule expression by nitric oxide donors and antioxidants , 1998, Journal of leukocyte biology.
[121] A. Aljada,et al. Insulin Inhibits Intranuclear Nuclear Factor κB and Stimulates IκB in Mononuclear Cells in Obese Subjects: Evidence for an Anti-inflammatory Effect? , 2001 .