Effects of the normal nocturnal increase in growth hormone on breakfast tolerance

Previous studies have shown that growth hormone (GH) excess causes insulin resistance. In order to determine whether physiologic changes in GH alter splanchnic and extrasplanchnic postprandial carbohydrate metabolism, 8 healthy subjects were studied twice. On one occasion GH was infused at a rate of 1 ng/kg/min to maintain constant "basal" GH throughout the night. On a second occasion, the "basal" GH infusion was supplemented by two additional GH infusions at a rate of 1 g/kg given over l hour at midnight and 2.30 a.m. to reproduce the normal nocturnal rise in GH. Endogenous GH secretion was inhibited on both occasions with octreotide. At 8 a.m. subjects were fed a mixed meal containing [2³H] glucose. [6³H] glucose and H¹⁴CO₃ were infused systemically in order to trace initial splanchnic glucose uptake, hepatic glucose release and ¹⁴CO₂ incorporation into glucose. Neither integrated postprandial glucose, insulin or C-peptide concentration nor glucose appearance or disappearance differed in the presence and absence of the nocturnal rise in GH. However, the nocturnal rise in GH appeared to alter the temporal pattern of metabolism. Glucose appearance during the initial 60 min following ingestion of the mixed meal was higher (P<0.02) primarily due to higher (P=0.07) meal appearance with no difference in hepatic glucose release or CO₂ incorporation into glucose (an index of gluconeogenesis). On the other hand the higher rates of appearance were compensated by higher rates of disappearance resulting in no net change in glucose concentration. Thus, while GH excess can cause insulin resistance, the normal nocturnal rise in GH does not appear to be an important regulator of postprandial carbohydrate metabolism.