Stress Hyperglycemia, Insulin Treatment, and Innate Immune Cells

Hyperglycemia (HG) and insulin resistance are the hallmarks of a profoundly altered metabolism in critical illness resulting from the release of cortisol, catecholamines, and cytokines, as well as glucagon and growth hormone. Recent studies have proposed a fundamental role of the immune system towar...

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Main Authors: Fangming Xiu, Mile Stanojcic, Li Diao, Marc G. Jeschke
Format: Article
Language:English
Published: Wiley 2014-01-01
Series:International Journal of Endocrinology
Online Access:http://dx.doi.org/10.1155/2014/486403
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author Fangming Xiu
Mile Stanojcic
Li Diao
Marc G. Jeschke
author_facet Fangming Xiu
Mile Stanojcic
Li Diao
Marc G. Jeschke
author_sort Fangming Xiu
collection DOAJ
description Hyperglycemia (HG) and insulin resistance are the hallmarks of a profoundly altered metabolism in critical illness resulting from the release of cortisol, catecholamines, and cytokines, as well as glucagon and growth hormone. Recent studies have proposed a fundamental role of the immune system towards the development of insulin resistance in traumatic patients. A comprehensive review of published literatures on the effects of hyperglycemia and insulin on innate immunity in critical illness was conducted. This review explored the interaction between the innate immune system and trauma-induced hypermetabolism, while providing greater insight into unraveling the relationship between innate immune cells and hyperglycemia. Critical illness substantially disturbs glucose metabolism resulting in a state of hyperglycemia. Alterations in glucose and insulin regulation affect the immune function of cellular components comprising the innate immunity system. Innate immune system dysfunction via hyperglycemia is associated with a higher morbidity and mortality in critical illness. Along with others, we hypothesize that reduction in morbidity and mortality observed in patients receiving insulin treatment is partially due to its effect on the attenuation of the immune response. However, there still remains substantial controversy regarding moderate versus intensive insulin treatment. Future studies need to determine the integrated effects of HG and insulin on the regulation of innate immunity in order to provide more effective insulin treatment regimen for these patients.
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spelling doaj-art-2502692c19034920955e7f690641c63a2025-02-03T06:13:56ZengWileyInternational Journal of Endocrinology1687-83371687-83452014-01-01201410.1155/2014/486403486403Stress Hyperglycemia, Insulin Treatment, and Innate Immune CellsFangming Xiu0Mile Stanojcic1Li Diao2Marc G. Jeschke3Ross Tilley Burn Centre, Sunnybrook Health Sciences Centre, University of Toronto, 2075 Bayview Avenue, Room D704, Toronto, ON, CanadaRoss Tilley Burn Centre, Sunnybrook Health Sciences Centre, University of Toronto, 2075 Bayview Avenue, Room D704, Toronto, ON, CanadaRoss Tilley Burn Centre, Sunnybrook Health Sciences Centre, University of Toronto, 2075 Bayview Avenue, Room D704, Toronto, ON, CanadaRoss Tilley Burn Centre, Sunnybrook Health Sciences Centre, University of Toronto, 2075 Bayview Avenue, Room D704, Toronto, ON, CanadaHyperglycemia (HG) and insulin resistance are the hallmarks of a profoundly altered metabolism in critical illness resulting from the release of cortisol, catecholamines, and cytokines, as well as glucagon and growth hormone. Recent studies have proposed a fundamental role of the immune system towards the development of insulin resistance in traumatic patients. A comprehensive review of published literatures on the effects of hyperglycemia and insulin on innate immunity in critical illness was conducted. This review explored the interaction between the innate immune system and trauma-induced hypermetabolism, while providing greater insight into unraveling the relationship between innate immune cells and hyperglycemia. Critical illness substantially disturbs glucose metabolism resulting in a state of hyperglycemia. Alterations in glucose and insulin regulation affect the immune function of cellular components comprising the innate immunity system. Innate immune system dysfunction via hyperglycemia is associated with a higher morbidity and mortality in critical illness. Along with others, we hypothesize that reduction in morbidity and mortality observed in patients receiving insulin treatment is partially due to its effect on the attenuation of the immune response. However, there still remains substantial controversy regarding moderate versus intensive insulin treatment. Future studies need to determine the integrated effects of HG and insulin on the regulation of innate immunity in order to provide more effective insulin treatment regimen for these patients.http://dx.doi.org/10.1155/2014/486403
spellingShingle Fangming Xiu
Mile Stanojcic
Li Diao
Marc G. Jeschke
Stress Hyperglycemia, Insulin Treatment, and Innate Immune Cells
International Journal of Endocrinology
title Stress Hyperglycemia, Insulin Treatment, and Innate Immune Cells
title_full Stress Hyperglycemia, Insulin Treatment, and Innate Immune Cells
title_fullStr Stress Hyperglycemia, Insulin Treatment, and Innate Immune Cells
title_full_unstemmed Stress Hyperglycemia, Insulin Treatment, and Innate Immune Cells
title_short Stress Hyperglycemia, Insulin Treatment, and Innate Immune Cells
title_sort stress hyperglycemia insulin treatment and innate immune cells
url http://dx.doi.org/10.1155/2014/486403
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AT milestanojcic stresshyperglycemiainsulintreatmentandinnateimmunecells
AT lidiao stresshyperglycemiainsulintreatmentandinnateimmunecells
AT marcgjeschke stresshyperglycemiainsulintreatmentandinnateimmunecells