[Septic shock: blood glucose regulation]

Abstract

Blood glucose regulation is controlled by several hormones, neurological mechanisms and the hepatic autoregulation. Glucose uptake necessitates glucose transporters which are called GLUT. In physiological situation, 80% of glucose uptake of the whole body is produced by the non-insulin dependant tissues, via the GLUT 1 to 3 transporters. Glucose uptake by insulin dependant tissues is mediated by insuline, which activates GLUT-4 transporters. Because of the production of pro-inflammatory mediators (TNF-alpha), sepsis induces hyperglycemia, which results essentially from an hepatic insulinoresistance. This phenomenon leads to an acute load and uptake of glucose by the non-insulin dependant tissues. Hyperglycemia modifies inflammatory and immune reactions and enhances the production of reactive oxygen species. Thus, sepsis has an impact on blood glucose control and conversely. Blood glucose control has been found to decrease mortality and morbidity in critically ill patients. The exact mechanism, by which these beneficial effects are produced, remains controversial, due to euglycemia or to insulin infusion. Probably both mechanisms are implicated. In all cases the beneficial effects seem to be multifactorial: a decrease in oxydative stress, a protective effect in front of the burst suppression, multiple anti-inflammatory effects. The optimum level of blood glucose is still discussed and must be evaluated in further studies. In all cases, blood glucose level must be under or equal to 1,4 g/l. Even no clinical study evaluates precisely the impact of hyperglycemia during sepsis, a lot of arguments supports that blood glucose level must be a therapeutic goal in these situations.