Preoperative feeding does not reverse postoperative insulin resistance in skeletal muscle in the rat

Metabolic studies on injured and postoperative patients have shown impaired glucose disposal in peripheral tissues after trauma. Using small-bowel res ection as a model of surgical trauma, we investigated whether substrate ava ilability could ameliorate the changes in muscle glucose uptake induced by trauma. We also studied the effect of preoperative feeding on postoperative insulin-stimulated insulin receptor substrate-1 (IRS-1)-associated phospha tidylinositol (PI) 3-kinase activity in both Wistar rats and genetically no n-insulin-dependent diabetic Goto-Kakazaki rats (GK rats). Serum glucose, I nsulin, plasma epinephrine, lactate, and plasma nonesterified free fatty ac ids (NEFAs) were measured as indicators of the metabolic state end surgical stress. insulin-stimulated glucose transport was significantly reduced in fed traumatized Wister rats compared with fed nontraumatized rats (P <.05). Significant increases in in vivo insulin-stimulated IRS-1-associated PI 3- kinase activity were found in fed traumatized Wistar mts compared with fed nontraumatized Wistar rats and fasted traumatized Wistar rats, as well as f ed traumatized GK rats compared with fed nontraumatized GK animals (all P < .017). Serum insulin concentrations were significantly reduced in fed traum atized Wistar and GK rats compared with the respective fed nontraumetized g roups (both P <.01). Serum glucose levels were significantly elevated in fe d traumatized GK rats compared with fed nontraumatized animals (P <.01). In the present study, preoperative feeding did not prevent a postoperative re duction In Insulin-stimulated glucose transport in skeletal muscle. The fin ding that insulin-stimulated PI 3-kinase activity increased after trauma in both Wister and GK rats indicates that postoperative insulin resistance is not caused by an Impairment in the early steps of the insulin signaling pa thway. The postoperative decreases in serum insulin despite high blood gluc ose suggest that trauma impairs the insulin response to hyperglycemia. Copy right (C) 2000 by W.B. Saunders Company.