The role of growth hormone in the glucose intolerance of uremia.

The fasting plasma growth hormone (GH) concentration and the plasma growth hormone response to sustained hyperglycemia was examined in 8 chronically uremic subjects before and after hemodialysis employing the hyperglycemia clamp technique. The plasma glucose concentration was acutely raised and maintained at +125 mg/100 ml above basal levels. Since the glucose concentration was held constant, the glucose infusion rate is an index of glucose metabolism (M) and M divided by the plasma insulin response (I) is a measure of tissue sensitivity to insulin. Predialysis, the fasting GH concentration, 4.0 +/- 1.0 ng/ml, was significantly greater than controls, 0.3 +/- 0.1 ng/ml (p less than 0.01), and failed to suppress normally following sustained hyperglycemia. Both M, 4.23 +/- 0.36 mg/kg x min, and M/I, 5.05 +/- 0.79 mg/kg x min per microU/ml, were significantly reduced compared to controls (p less than 0.001). There was no correlation between either the fasting GH concentration or the GH response to sustained hyperglycemia and either M or M/I. Following dialysis both M, 6.30 +/- 0.64 mg/kg x min, and M/I, 8.39 +/- 1.06 mg/kg x min per microU/ml, increased (p less than 0.01) without significant change in either the fasting GH level, 4.0 +/- 1.2 ng/ml, or the plasma GH response to hyperglycemia. It is concluded that while deranged GH physiology is a common accompaniment of the uremic state, it is not responsible for the glucose intolerance and tissue insensitivity to insulin observed in uremia.