Insulin in the critically ill with focus on cytokines, reactive oxygen species, HLA-DR expression.

Abstract

Insulin is essential for glucose homeostasis. Insulin/glucose-insulin-potassium (GIK) regimen suppresses the production of tumor necrosis factor-alpha (TNF-alpha), interleukins-6 (IL-6), macrophage migration inhibitory factor (MIF) and other pro-inflammatory cytokines and reactive oxygen species (ROS), enhances the synthesis of endothelial nitric oxide (eNO), and anti-inflammatory cytokines interleukins-4 (IL-4) and interleukin-10 (IL-10). In subjects who are critically ill, monocyte HLA-DR expression was significantly decreased with a concomitant increase in plasma IL-10 and IL-4 concentrations. Large increases in the plasma concentrations of TNF-alpha, IL-6, sustained increase in the expression of leukocyte CD11b/CD18, and ROS generation following surgery and infections were found to be associated with increased mortality. By virtue of its actions on pro- and anti-inflammatory cytokines and ROS, insulin may have the ability to alter HLA-DR expression in the critically ill and thus bring about its beneficial actions in sepsis/septic shock, myocardial recovery following acute myocardial infarction, improve prognosis of those who are critically ill, and suppress inflammation.

• Authors: Undurti N Das
• Journal: The Journal of the Association of Physicians of India (J Assoc Physicians India) Vol. 55 Suppl Pg. 56-65 (Jul 2007) ISSN: 0004-5772 [Print] India
• PMID: 17927013 (Publication Type: Journal Article, Review)

Chemical References

• Cytokines
• HLA-DR Antigens
• Insulin
• Reactive Oxygen Species
• Nitric Oxide

Topics

• Critical Illness
• Cytokines (drug effects)
• Diabetes Mellitus (prevention & control)
• Endothelium (drug effects)
• HLA-DR Antigens (biosynthesis, drug effects)
• Humans
• Hyperglycemia (prevention & control)
• Insulin (pharmacology, therapeutic use)
• Nitric Oxide
• Reactive Oxygen Species