Preoperative oral carbohydrate treatment attenuates endogenous glucose release 3 days after surgery

Protein and amino acid metabolism after injury

After reviewing our current knowledge of the metabolic response to major abdominal surgery, we present two new studies in which we have followed the changes in body composition, physiologic function, and psychological function for up to 1 year after major surgery. In the first study, 46 patients had changes in body composition, physiologic function, and psychological function measured perioperatively and again at intervals up to 1 year. There was an average loss of weight of 3000 grams (maximum at 2 weeks), and the tissue composition of this weight loss was composed of 1400 grams fat, 600 grams protein, and 1000 grams water. Normal body composition had returned to normal in most patients by 6 months. In the second study of 84 patients, deficits of skeletal muscle function and fatigue were found to be greatest at postoperative day 7. Most patients were back to preoperative levels of muscle function and fatigue 30 days after surgery, and nearly all had normal values 90 days after surgery. Based on these studies we outline our management program for the metabolic care of patients undergoing major abdominal surgery.

Metabolic basis for the management of patients undergoing major surgery.

https://www.advancessurgery.com/article/S0065-3411(05)00018-7/pdf

The pharmacologic modulation of the hypermetabolic response to burns.

Hyperglycemia is an early metabolic response to trauma and hemorrhage. The role of hepatic insulin resistance to the development of this hyperglycemia is not well understood. The aim of this study was to determine whether the liver becomes insulin resistant and to identify the particular hepatic insulin signaling pathways that may be compromised following trauma and hemorrhage. Male adult rats were bled to a mean arterial pressure of 40 mmHg and maintained at that pressure for 90 min followed by resuscitation with Ringer lactate. Data showed that trauma and hemorrhage rapidly induced profound hyperinsulinemia in combination with significant hyperglycemia, suggesting the development of insulin resistance. After trauma and hemorrhage, hepatic insulin signaling via the insulin-induced phosphatidylinositol 3 (PI3)-kinase-Akt pathway was abolished, whereas ERK1/2 signaling was relatively normal. The regulation (inhibition) of a hepatic-, insulin-, and the PI3-kinase-dependent gene, IGF binding protein-1, was also lost. The present study provides convincing evidence of a rapid onset hepatic insulin resistance following a combination of trauma and hemorrhage.

https://www.physiology.org/doi/pdf/10.1152/ajpgi.00217.2002

Hemorrhage induces the rapid development of hepatic insulin resistance.

Insulin decreases muscle protein loss after operative trauma in man.

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Insulin decreases muscle protein loss after operative trauma in man.