Horm Metab Res 1982; 14(1): 34-39
DOI: 10.1055/s-2007-1018914
© Georg Thieme Verlag, Stuttgart · New York

Hormonal and Metabolic Changes in Hepatic Cirrhosis

D. G. Johnston1 , K. G. M. M. Alberti1 , C. Binder2 , O. K. Faber2 , R. Wright3 , H. Orskov4
  • 1Departments of Medicine and Clinical Biochemistry, Royal Victoria Infirmary, Newcastle upon Tyne, U.K.
  • 2Steno Memorial Hospital, Gentofte, Denmark
  • 3Department of Medicine, General Hospital, Southampton, U.K.
  • 42 Medicinske Universitetsklinik, Kommune Hospitalet, Aarhus, Denmark
Weitere Informationen

Publikationsverlauf

1980

1981

Publikationsdatum:
14. März 2008 (online)

Summary

The hormonal and metabolic response to 50 g oral glucose has been studied in fifteen patients with hepatic cirrhosis and seven control subjects. Fasting blood glucose concentration was similar in both groups but cirrhotics showed higher glucose levels throughout the glucose tolerance test. Fasting serum insulin concentration was raised in the patient group (0.12 ± 0.02 vs 0.07 ± 0.01 nmol/l, p < 0.05) and hyperinsulinaemia persisted after oral glucose. Blood lactate and pyruvate concentrations were elevated in cirrhotic patients, both fasting and post-glucose, while mean blood lactate correlated with mean serum insulin concentrations (rs 0.55, p < 0.05). Plasma glucagon concentrations although highly variable, did not differ significantly in control and cirrhotic subjects before or after oral glucose. Fasting blood glycerol was increased in the patient group (0.11 ± 0.01 vs 0.06 ± 0.01 mmol/l, p < 0.05) but fasting blood ketone body levels were normal and both glycerol and ketone body concentrations fell normally after glucose. Basal serum cortisol levels were similar in patient and control groups but the expected fall in cortisol concentration found in the control group over the test period was absent in cirrhotics. The hormonal and metabolic abnormalities did not correlate with severity of disease assessed by liver function tests and abnormalities were not related to the presence or absence of portal-systemic shunting.

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