125I-insulin binding to monocytes was examined in five children and one adult with isolated growth hormone deficiency before and after three to 12 weeks of growth hormone treatment, and in eight controls. Before treatment, mean plasma glucose was 15 mg per deciliter below controls, and plasma insulin was reduced by 40 per cent. Insulin binding to monocytes was 70 per cent greater than controls (P<0.005). Insulin-mediated glucose uptake (determined in the adult patient) was 25 per cent greater than mean control levels. After treatment, plasma glucose rose to control levels, plasma insulin increased to 75 per cent above controls (P<0.01), and insulin binding fell to 50 per cent below controls (P<0.01). Insulin-mediated glucose uptake fell to 30 per cent below the mean control rate. Insulin binding increases in growth hormone deficiency and falls after treatment. These changes may contribute to alterations in insulin sensitivity accompanying altered growth hormone availability. (N Engl J Med 299:1025–1030, 1978) HUMAN growth hormone is known to alter tissue responsiveness to insulin. In clinical practice this effect is exemplified by a tendency to fasting hypoglycemia and augmented sensitivity to insulin in patients with isolated growth hormone deficiency,12 and glucose intolerance in association with hyperinsulinemia and insulin resistance in patients with acromegaly.3 The cellular mechanism of these changes in insulin sensitivity accompanying altered secretion of growth hormone has not been established. Recently, changes in insulin binding have been implicated in the altered insulin sensitivity of obesity,4 uremia5 and maturity-onset diabetes.6 In addition, physiologic stimuli like glucose ingestion7 and exercise8 have been shown.
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