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

M. F. Nielsen, S. Dinneen, A. Basu, A. Alzaid, R. A. Rizza

Research output: Contribution to journalArticlepeer-review


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 mg/kg given over 1 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 HI4CO3 were infused systemically in order to trace initial splanchnic glucose uptake, hepatic glucose release and I4CO2 incorporation into glucose. Indirect calorimetry was performed in order to assess carbohydrate and lipid oxidation. 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 (Ra) during the initial 60 min following ingestion of the mixed meal was higher (PO.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. No difference in plasma FFA concentrations or in carbohydrate and lipid oxidation could be demonstrated between groups. 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.

Original languageEnglish (US)
Pages (from-to)260a
JournalJournal of Investigative Medicine
Issue number3
StatePublished - 1996

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology


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