Daxu Peng
Department of Intensive Care Unite, North China University of Science and Technology Affiliated Hospital, Tangshan, Hebei, 063000, China
Yifan Zhang
Department of Intensive Care Unite, North China University of Science and Technology Affiliated Hospital, Tangshan, Hebei, 063000, China
Xiuyang Cao
Department of Hepatobiliary Surgery, North China University of Science and Technology Affiliated Hospital, Tangshan, Hebei, 063000, China
Jianyi Pu
Department of Intensive Care Unite, North China University of Science and Technology Affiliated Hospital, Tangshan, Hebei, 063000, China
Stress hyperglycemia is a strong neuroendocrine reaction in thehypothalamic pituitary adrenal cortex under severe infection, trauma, burns,hemorrhage, surgery and other harmful stimulated, resulting in increasedsecretion of counter-regulatory hormones. These hormones promotedthe production of sugar and cause glucose metabolism disorders withcytokines and insulin resistance. In this condition, the production of sugarexceeds the utilization of sugar by the tissues, which eventually leads to anincrease in blood glucose levels in plasma. In the intensive care unit, stresshyperglycemia is very common and can occur in patients with or withoutdiabetes. The incidence is as high as 96%, and it is an independent factorin the death of critically ill patients. Hyperglycemia not only prolongsthe hospitalization time, mechanical ventilation time and increased theincidence of serious infections in critically ill patients, but can also leadto the occurrence of type 2 diabetes. Therefore, it is very important tolearn the pathological mechanism of stress hyperglycemia, the harm ofhyperglycemia and blood sugar management.
[1] Mechanick, J.I., 2006. Metabolic mechanisms of stress hyperglycemia. Journal of parenteral and Enteral Nutrition. 30(2), 157-163.
[2] Chu, Z., Takagi, H., 2010. Hyperpolarization-activated currents in gonadotropin-releasing hormone (GnRH) neurons contribute to intrinsic excitability and are regulated by gonadal steroid feedback. The Journal of neuroscience : the official journal of the Society for Neuroscience. 30, 13373-13383.
[3] Marfella, R., Siniscalchi, M., Esposito, K., et al., 2003. Effects of stress hyperglycemia on acute myocardial infarction: role of inflammatory immune process in functional cardiac outcome. Diabetes care. 26(11), 3129-3135.
[4] Harp, J.B., Yancopoulos, G.D., 2016. Glucagon orchestrates stress-induced hyperglycaemia. Diabetes, obesity & metabolism. 18, 648-653.
[5] Sprung, C.L., Annane, D., Singer, M., et al., 2009. Steroids in patients with septic shock. Chest. 136(1), 323-324.
[6] Chernow, B., Rainey, T.G., Lake, C.R., 1982. Endogenous and exogenous catecholamines in critical care medicine. Critical Care Medicine. 10(6), 409-416.
[7] Tziomalos, K., Dimitriou, P., Bouziana, S.D., et al., 2017. Stress hyperglycemia and acute ischemic stroke in-hospital outcome. Metabolism. 67(9), 99- 105.
[8] Barth, E., Albuszies, G., Baumgart, K., et al., 2007. Glucose metabolism and catecholamines. Critical care medicine. 35(9), S508-S518.
[9] Fan, J., Li, Y.H., Wojnar, M.M., et al., 1996. Endotoxin-induced alterations in insulin-stimulated phosphorylation of insulin receptor, IRS-1, and MAP kinase in skeletal muscle. Shock (Augusta, Ga.). 6(3), 164-170.
[10] Lang, C.H., Dobrescu, C., MEszAros, K., 1990. Insulin-mediated glucose uptake by individual tissues during sepsis. Metabolism. 39(10), 1096-1107.
[11] Dresner, A., Laurent, D., Marcucci, M., et al., 1999. Effects of free fatty acids on glucose transport and IRS-1–associated phosphatidylinositol 3-kinase activity. The Journal of clinical investigation. 103(2), 253-259.
[12] Voeltz, G.K., Rolls, M.M., Rapoport, T.A., 2002. Structural organization of the endoplasmic reticulum[J]. EMBO reports. 3(10), 944-950.
[13] Braakman, I., Bulleid, N.J., 2011. Protein folding and modification in the mammalian endoplasmic reticulum. Annual review of biochemistry. 80(2), 71-99.
[14] Ibrahim, I.M., Abdelmalek, D.H., Elfiky, A.A., 2019. GRP78: a cell’s response to stress. Life sciences. 226(23), 156-163.
[15] Pfaffenbach, K.T., Lee, A.S., 2011. The critical role of GRP78 in physiologic and pathologic stress. Current opinion in cell biology. 23(2), 150-156.
[16] Hendershot, L.M., 2004. The ER function BiP is a master regulator of ER function. The Mount Sinai journal of medicine, New York. 71(5), 289-297.
[17] Ghemrawi, R., Battaglia, S.F., Arnold, C., 2018. Endoplasmic reticulum stress in metabolic disorders. Cells. 7(6), 63-70.
[18] Pandey, V.K., Mathur, A., Kakkar, P., 2019. Emerging role of Unfolded Protein Response (UPR) mediated proteotoxic apoptosis in diabetes. Life sciences. 216(6), 246-258.
[19] Ubeda, M., Wang, X.Z., Zinszner, H., et al., 1996. Stress-induced binding of the transcriptional factor CHOP to a novel DNA control element. Molecular and cellular biology. 16(4), 1479-1489.
[20] Matsumoto, M., Minami, M., Takeda, K., et al., 1996. Ectopic expression of CHOP (GADD153) induces apoptosis in M1 myeloblastic leukemia cells. FEBSletters. 395(2), 143-147.
[21] Nam, D.H., Han, J.H., Lee, T.J., et al., 2015. CHOP deficiency prevents methylglyoxal-induced myocyte apoptosis and cardiac dysfunction. Journal of molecular and cellular cardiology. 85(1), 168-177.
[22] Yao, Y., Lu, Q., Hu, Z., et al., 2017. A non-canonical pathway regulates ER stress signaling and blocks ER stress-induced apoptosis and heart failure. Nature communications. 8(1), 1-15.
[23] Oyadomari, S., Mori, M., 2004. Roles of CHOP/ GADD153 in endoplasmic reticulum stress. Cell Death & Differentiation. 11(4), 381-389.
[24] Tu, B.P., 2004. Weissman J S. Oxidative protein folding in eukaryotes mechanisms and consequences. Journal of Cell Biology. 164(3), 341-346.
[25] Santos, C.X.C., Tanaka, L.Y., Wosniak, Jr.J., et al., 2009. Mechanisms and implications of reactive oxygen species generation during the unfolded protein response: roles of endoplasmic reticulum oxidoreductases, mitochondrial electron transport, and NADPH oxidase. Antioxidants & redox signaling. 11(10), 2409-2427.
[26] Hwang, C., Sinskey, A.J., Lodish, H.F., 1992. Oxidized redox state of glutathione in the endoplasmic reticulum. Science. 257(5076), 1496-1502.
[27] Rao, J., Zhang, C., Wang, P., et al., 2015. C/EBP homologous protein (CHOP) contributes to hepatocyte death via the promotion of ERO1α signalling in acute liver failure. Biochemical Journal. 466(2), 369-378.
[28] Li, G., Scull, C., Ozcan, L., et al., 2010. NADPH oxidase links endoplasmic reticulum stress, oxidative stress, and PKR activation to induce apoptosis. Journal of Cell Biology. 191(6), 1113-1125.
[29] Brand, M.D., 2010. The sites and topology of mitochondrial superoxide production. Experimental gerontology. 45(7), 466-472.
[30] Carreras-Sureda, A., PihAn, P., Hetz, C., 2018. Calcium signaling at the endoplasmic reticulum: fine-tuning stress responses. Cell Calcium. 70(12), 24-31.
[31] GOrlach, A., Klappa, P., Kietzmann, D.T., 2006. The endoplasmic reticulum: folding, calcium homeostasis, signaling, and redox control. Antioxidants & redox signaling. 8(9), 1391-1418.
[32] St-Pierre, J., Buckingham, J.A., Roebuck, S.J., et al., 2002. Topology of superoxide production from different sites in the mitochondrial electron transport chain. Journal of Biological Chemistry. 277(47), 44784-44790.
[33] Men, X., Wang, H., Li, M., et al., 2009. Dynamin-related protein 1 mediates high glucose induced pancreatic beta cell apoptosis. The international journalof biochemistry & cell biology. 41(4), 879-890.
[34] Wang, M., Liu, Y., Liang, Y., et al., 2021. Systematic understanding of pathophysiological mechanisms of oxidative stress-related conditions—diabetes mellitus, cardiovascular diseases, and ischemia–reperfusion injury. Frontiers in Cardiovascular Medicine. 4(8), 649785.
[35] Burgos-Morón, E., Abad-Jiménez, Z., Martinez de Maranon, A., et al., 2019. Relationship between oxidative stress, ER stress, and inflammation in type 2 diabetes: the battle continues. Journal of clinical medicine. 8(9), 1385.
[36] Kerby, J.D., Griffin, R.L., MacLennan, P., et al., 2012. Stress-induced hyperglycemia, not diabetic hyperglycemia, is associated with higher mortality in trauma. Annals of surgery. 256(3), 446-452.
[37] Clement, S., Braithwaite, S.S., Magee, M.F., et al., 2004. Management of diabetes and hyperglycemia in hospitals. Diabetes care. 27(2), 553-591.
[38] Yang, Z., Laubach, V.E., French, B.A., et al., 2009. Acute hyperglycemia enhances oxidative stress and exacerbates myocardial infarction by activating nicotinamide adenine dinucleotide phosphate oxidase during reperfusion. The Journal of thoracic and cardiovascular surgery. 137(3), 723-729.
[39] Chen, Y., Yang, X., Meng, K., et al., 2013. Stress-induced hyperglycemia after hip fracture and the increased risk of acute myocardial infarction in nondiabetic patients. Diabetes care. 36(10), 3328-3332.
[40] Sonneville, R., den Hertog, H.M., GUiza, F., et al., 2012. Impact of hyperglycemia on neuropathological alterations during critical illness. The Journal of Clinical Endocrinology & Metabolism. 97(6), 2113-2123.
[41] Vanhorebeek, I., Gunst, J., Ellger, B., et al., 2009. Hyperglycemic kidney damage in an animal model of prolonged critical illness. Kidney international. 76(5), 512-520.
[42] Kavanagh, B.P., McCowen, K.C., 2010. Glycemic control in the ICU. New England Journal of Medicine. 363(26), 2540-2546.
[43] Umpierrez, G.E., Hellman, R., Korytkowski, M.T., et al., 2012. Management of hyperglycemia in hospitalized patients in non-critical care setting: an endocrine society clinical practice guideline. The Journal of Clinical Endocrinology & Metabolism. 97(1), 16-38.
[44] Jacobi, J., Bircher, N., Krinsley, J., et al., 2012. Guidelines for the use of an insulin infusion for the management of hyperglycemia in critically ill patients. Critical care medicine. 40(12), 3251-3276.
[45] Ali, N.A., O’Brien, Jr.J.M., Dungan, K., et al., 2008. Glucose variability and mortality in patients with sepsis. Critical care medicine. 36(8), 2316.
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