Propriétés anti-inflammatoires de l'insuline chez les patients en réanimation

Critically ill patients requiring intensive care for more than a few days have a high risk of death. A tight control of glucose levels by intense insulin therapy reduced morbidity in critically ill patients. Insulin acts by two major molecular pathways: a. reduction of inflammation process induced by free fatty acids excess in tissues b. decrease of reactive oxygen species (ROS) production induced by hyperglycemia. By these actions, insulin preserve mitochondrial function, enhances adiponectin secretion and probably modulates AMP-activated protein kinase activity, which in turn depletes lipids depots in tissues and restores glucose uptake and oxidation. Furthermore, it has been recently established that insulin prevents microcirculation alteration and subsequent cellular hypoxia by reducing iNOS expression and activity in endothelium. So, beneficial effects of insulin in critically ill patients are dependent on metabolic and non-metabolic molecular pathways.