Alterations in fuel metabolism in stress

Abstract

The hyperglycaemia and glucose intolerance observed in patients following severe trauma appear to be central to the metabolic response to injury. Oral and intravenous glucose tolerance tests following injury^1,2, burn shock^2,3 and systemic infection^5,6 demonstrated delayed disposal of glucose from the plasma into body tissues. Hyperglycaemia and the increased urinary nitrogen losses in these patients were consistent with an insulin-deficient state and terms such as ‘stress diabetes’ or the ‘diabetes of injury’ were used to describe this metabolic response to injury. Although it has been shown that during the early or ‘ebb’ phase of injury hypoinsulinaemia does exist^1,3,7, following resuscitation, as the patient enters the ‘flow’ phase of injury, the beta cell response to glucose load is normal or even higher than that observed in normals^3,7. Hyperglycaemia and glucose intolerance in the presence of a normal or increased insulin response would suggest that certain target tissues of the injured patient are relatively resistant to circulating insulin. The aetiology of the resistance to circulating insulin in the injured patient is not presently known. However, recent advances made in insulin physiology have produced a clearer understanding of the insulin resistance following injury.