Effect of traumatic injury on sensitivity to insulin.
Disturbances in carbohydrate homeostasis are metabolic hallmarks in the host response to trauma. Since alterations in insulin responsiveness, especially insulin resistance, have been related to the metabolic sequelae of shock, the present study evaluated insulin responsiveness in traumatic shock. Injury (LD50) of fasted, male Holtzman rats (115 plus or minus 20 gm) by tumbling in the Noble-Collip drum resulted in hyperglycemia in spite of a concomitant hyperinsulinemia. The ability of insulin to lower plasma glucose was evaluated at either three hours or 24 hours post-trauma by means of glucose and insulin tolerance tests. The injured rats showed glucose intolerance and hyperinsulinemia three hours after injury but showed a normal glucose tolerance and hypoinsulinemia on the day after injury. Insulin was ineffective in lowering plasma glucose at both of these times. Noble-Collip tumbling trauma induced no systemic changes in insulin responsiveness in vitro at either time as evaluated by 1) epididymal fat pad glucose oxidation of U-D-14C-glucose to 14CO2 or 2) hemidiaphragm incorporation of U-D-14C-glucose into glycogen. The data suggest that insulin resistance is not due to a decreased capacity of various tissues to respond to insulin.
D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose; D005947:Glucose / Q000378:metabolism; D005951:Glucose Tolerance Test; D007328:Insulin / Q000097:blood / Q000494:pharmacology*; D008297:Male; D009132:Muscles / Q000378:metabolism; D051381:Rats; D013997:Time Factors; D014947:Wounds and Injuries / Q000097:blood*
D001786:Blood Glucose; D007328:Insulin; D005947:Glucose