Insulin resistance and surgical stress

Abstract

Surgical procedures are associated with stress reaction, that leads to inflammation and insulin resistance. Insulin resistance is protective mechanism developed in postoperative period, in order to protect sources of carbohydrate for glucose-dependent organs, such as brain. Surgery, and other types of tissue traumatization, increase metabolism, oxidative processes and catabolic reactions as degradation of glycogen, fats and proteins. Insulin resistance occurs in extra hepatic tissue, especially in skeletal muscles. The degree of insulin resistance and its duration, depends of tissue damage. Less invasive surgical interventions induce weaker inflammatory response, shorter decrease in insulin sensitivity, less number of postoperative complications (infections and cardiovascular complications), followed by shorter postoperative hospitalization. Interleukin 6 (IL-6) and Tumor necrosis factor alpha (TNF-alpha) are increased in postoperative period, as well as C-reactive protein (CRP), marker of inflammation. Preoperative glucose infusion with insulin leads to less catabolic effect, and has positive effect on insulin sensitivity. The level of insulin resistance, irrespective of type of surgery, has direct influence on duration of hospital stay and postoperative complications. Postoperative surgical stress and postoperative insulin resistance could be lowered by minimal invasive surgery.

Keywords

• Insulin resistance
• surgical stress
• inflammation parameters
• IL-6
• CRP