This paper describes a new method for evaluating glucose metabolism in man using an oral glucose load. The procedure permits the calculation of a blood glucose disappearance rate constant (K) and thereby makes it possible to compare quantitatively the response to oral and intravenous glucose administration in a given individual. Ten metabolically normal adult humans were studied under carefully controlled conditions. Each received similar amounts (20 g) of glucose both orally and intravenously (2-7 days apart) by constant infusion for 1 hr. The effects on blood glucose disappearance rate constants (K) and plasma insulin concentrations (immunoassay) during and for 1 hr following the infusion were compared. Blood glucose concentrations and K values with the 2 routes of glucose administration were similar. In contrast, plasma insulin responses showed a significant difference: oral glucose resulted in a significant and sustained rise, whereas intravenous glucose was associated with a smaller and transient increase.The plasma insulin increase with intravenous glucose is considered to be due to the wellknown effect of hyperglycemia on insulin secretion. The greater and more sustained increase in plasma insulin with oral glucose is interpreted as evidence for an additional stimulus to insulin secretion, possibly a gastrointestinal or liver factor triggered by alimentary glucose. (J Clin Endocr 24: 1076, 1964 B OTH ORAL and intravenous glucose tolerance tests are widely used to evaluate glucose metabolism in man. Intravenous methods permit the calculation of a specific rate constant for glucose utilization (K) from a relationship of blood glucose and time, whereas present oral methods do not allow for such a quantitative expression of data and are handicapped by the variable of intestinal absorption. Thus, there are no published reports on a quantitative comparison of oral and intravenous glucose utilization in man.This paper describes a new method for

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A B S T R A C T The effects of administered human growth hormone (HGH) were evaluated in dwarfed, prepubertal children who were receiving long-term corticosteroid therapy for a chronic disease. During 11 complete metabolic balance studies, the eight corticosteroid-treated children demonstrated impaired response to large doses of HGH with minimal nitrogen and no phosphorus retention. In contrast, two hypopituitary subjects and two asthmatic children not receiving corticosteroid responded to the same preparations of HGH with nitrogen, potassium, and phosphorus retention. Six corticosteroid-treated children were given large doses of HGH (40-120 mg/wk for 4 to 8 months and showed no improvement in their retarded rate of growth, whereas the hypopituitary subjects showed accelerated growth during administration of 10-15 mg of HGH/wk. It is concluded that dwarfism in steroid-treated children results from corticosteroid-induced antagonism of the effects of HGH at the peripheral tissue level.

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