Post-traumatic insulin resistance in uninjured forearm tissue.

Insulin resistance is a hallmark of post-traumatic metabolism. The mechanism and site of this resistance, however, have not been elucidated. To further define the site of this abnormality, glucose uptake across the uninjured forearm was measured in conjunction with hyperinsulinemic glucose clamp studies in 21 normals and 5 patients with multiple trauma. Under these conditions, glucose infused approximates whole body glucose disposal (M, milligrams/kilogram/min). Forearm glucose flux (Q, milligrams/100 ml tissue/min) is the product of blood flow and arterial-deep venous glucose difference (A-DV). In the basal, unperturbed state forearm glucose uptake (Q) was significantly lower in the patients (0.01 +/- 0.04 mg/100 ml/min) than in the normals (0.06 +/- 0.02) and not significantly different from zero. Basal serum insulin in patients (17 +/- 3 microU/ml) was significantly greater than controls (11 +/- 1). During steady-state conditions of euglycemia and hyperinsulinemia, forearm glucose uptake in the patients (0.36 +/- 0.18 mg/100 ml/min was not significantly different from the basal value. At comparable serum insulin levels in controls, forearm glucose uptake was approximately three times that of the injured patients. This is the first in vivo confirmation of the hypothesis that post-traumatic insulin resistance occurs in uninjured forearm tissue, primarily skeletal muscle. Diminished forearm glucose uptake is present in the resting basal state and cannot be overcome by increasing insulin concentrations.