The cirrhotic liver has been shown to be resistant to the actions of v
arious glucoregulatory hormones. The objective of this study was to in
vestigate the effects of epinephrine on hepatic glucose metabolism in
cirrhotic patients, Thirteen cirrhotic and eight healthy subjects were
studied. Hepatic glucose production and turnover of alanine and glyce
rol were measured using stable isotope technique before and during 70
and 150 minutes of epinephrine infusion (0.1 mu g/kg/min). beta-Adreno
receptor binding sites and affinity in mononuclear leukocyte membranes
also were determined Hepatic glucose production and alanine turnover
in normals significantly increased during epinephrine infusion, but di
d not change in cirrhotics, Glycerol turnover increased after 70 minut
es of epinephrine infusion in both groups. Epinephrine induced a signi
ficant rise of high-affinity beta-adrenoreceptor binding sites in norm
als, yielding a significant correlation between hepatic glucose produc
tion and receptor density (r = .94, P < .0001). in cirrhotic patients,
similar changes in the number of high-affinity beta-adrenoreceptors w
ere observed but no correlation with hepatic glucose production was de
tected, The cirrhotic fiver did not respond normally to the stimulator
y effect of epinephrine on hepatic glucose production Because this blu
nted response was not related to changes of beta-adrenoreceptors, our
findings suggest that epinephrine resistance in cirrhosis was caused b
y a postreceptor defect.