Diabetologia

, Volume 20, Issue 2, pp 123–128

Metabolic effects of acute and prolonged growth hormone excess in normal and insulin-deficient man

Authors

  • P. Metcalfe
    • Southampton University Medical School
  • D. G. Johnston
    • Department of MedicineRoyal Victoria Infirmary
  • R. Nosadini
    • Departments of Clinical Biochemistry and Metabolic MedicineRoyal Victoria Infirmary
  • H. Ørksov
    • Afdeling MKommunehospitalet
  • K. G. M. M. Alberti
    • Departments of Clinical Biochemistry and Metabolic MedicineRoyal Victoria Infirmary
Originals

DOI: 10.1007/BF00262014

Cite this article as:
Metcalfe, P., Johnston, D.G., Nosadini, R. et al. Diabetologia (1981) 20: 123. doi:10.1007/BF00262014

Summary

The metabolic effects of acute (4 h) and prolonged (24 h) growth hormone excess at pathophysiological concentrations were studied by growth hormone administration to normal subjects with and without somatostatin induced insulin deficiency. Acute growth hormone excess produced mild hyperinsulinaemia, but blood glucose concentrations were unaltered whereas chronic growth hormone excess caused a small (0.5 mmol/l) but significant rise in overnight-fasting blood glucose concentration together with a similar rise in fasting insulin levels (Mean ± SEM 9 ± 1 v 4 ± 1 mU/l, p<0.01). When insulin secretion was suppressed by somatostatin, a hyperglycaemic effect of acute growth hormone excess was unmasked, and the hyperglycaemic effect of chronic growth hormone excess was exaggerated. Acute growth hormone administration without somatostatin had a mild ketogenic action despite stimulated insulin secretion but no change in plasma non-esterified fatty acid or blood glycerol levels was observed. Somatostatin magnified the ketogenic effect of acute growth hormone excess, and unmasked a lipolytic action. Prolonged growth hormone excess had a lipolytic action that was increased by somatostatin, although the ketogenic effect of growth hormone was only seen during somatostatin induced insulin deficiency. The acute hyperglycaemic, lipolytic and ketogenic actions of growth hormone in normal subjects are limited by a compensatory rise in insulin secretion although with chronic exposure hyperglycaemic and lipolytic effects are seen. In insulin-deficient states, however, elevated growth hormone levels could be important in promoting hyperglycaemia and hyperketonaemia.

Key words

Growth hormone insulin insulin deficiency glucagon blood glucose ketone bodies ketogenesis lipolysis non-esterified fatty acids

Copyright information

© Springer-Verlag 1981