Insulin Effects on Glucose Tolerance, Hypermetabolic Response, and Circadian-metabolic Protein Expression in a Rat Burn and Disuse Model.

摘要

Insulin controls hyperglycemia after severe burns, and its use opposes the hypermetabolic response. The underlying molecular mechanisms are poorly understood, and previous research in this area has been limited because of the inadequacy of animal models to mimic the physiological effects seen in humans with burns. Using a recently published rat model that combines both burn and disuse components, we compare the effects of insulin treatment vs. vehicle on glucose tolerance, hypermetabolic response, muscle loss, and circadian-metabolic protein expression after burns. hypermetabolism is a profoundly debilitating consequence of severe burns and is characterized by insulin resistance, hyper- glycemia, protein and lipid catabolism, total body protein loss, muscle wasting, elevated temperature, tachycardia, and high- energy requirements that last up to a year after injury (23, 27, 34).