Reduced thermic response after a glucose load has been reported in liv
er cirrhosis. To determine the mechanism and the site of this phenomen
on, the effects of glucose and fructose on energy expenditure (EE) wer
e measured in seven well-nourished cirrhotic patients and in six healt
hy control subjects. EE and fuel utilization were measured via indirec
t calorimetry for 3 h after oral glucose or fructose administration (1
g/kg body wt). After a glucose load, plasma glucose and insulin conce
ntrations were higher in cirrhotic patients than in control subjects (
p < 0.05). During the glucose trial, the cumulative incremental change
s in EE over the 3-h measurement period were lower (p < 0.01) in patie
nts than in the control subjects (0.98 +/- 0.13 vs. 1.70 +/- 0.23 kJ .
kg(-1) . 3 h(-1)). After fructose ingestion, the cumulative changes i
n the EE of control subjects (1.76 +/- 0.24 k . kg(-1) . 3 h(-1)) and
cirrhotic patients (1.59 +/- 0.15 kJ . kg(-1) . 3 h(-1)) were similar.
In cirrhotic patients, the EE increase after fructose was higher than
after glucose (p < 0.05). After glucose and fructose ingestion, no di
fference was observed between the carbohydrate oxidation in cirrhotic
patients and that in control subjects, and lipid oxidation was suppres
sed to the same extent in both groups. We conclude that glucose-induce
d thermogenesis is impaired in liver cirrhosis, whereas fructose can n
ormalize the thermic response. Because fructose is chiefly metabolized
in the liver, these findings suggest that extrahepatic tissues are th
e site of defective thermogenesis in liver cirrhosis.