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International Journal of Endocrinology
Volume 2014 (2014), Article ID 486403, 9 pages
Review Article

Stress Hyperglycemia, Insulin Treatment, and Innate Immune Cells

1Ross Tilley Burn Centre, Sunnybrook Health Sciences Centre, University of Toronto, 2075 Bayview Avenue, Room D704, Toronto, ON, Canada
2Sunnybrook Research Institute, University of Toronto, Toronto, ON, Canada M4N 3M5
3Department of Surgery, Division of Plastic Surgery, Department of Immunology, University of Toronto, Toronto, ON, Canada

Received 28 January 2014; Revised 6 April 2014; Accepted 8 April 2014; Published 8 May 2014

Academic Editor: Kristin Eckardt

Copyright © 2014 Fangming Xiu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.