Carbohydrate-induced thermogenesis in liver cirrhosis: glucose vs. fructose

• Published in: Nutrition (Burbank, Los Angeles County, Calif.) Vol. 10; no. 6; p. 521
• Main Authors: Martines, D, Martines, V, Pasini, M, Cocco, G, Lora, L, Varnier, M, Venier, G B, Sammartano, G, Naccarato, R
• Format: Journal Article
• Language: English
• Published: United States 01-11-1994
• Subjects: Administration, Oral; Adult; Aged; Blood Glucose - analysis; Body Temperature Regulation - drug effects; Calorimetry, Indirect; Cross-Over Studies; Energy Metabolism - physiology; Fatty Acids, Nonesterified - blood; Fructose - administration & dosage; Fructose - blood; Fructose - pharmacology; Glucose - administration & dosage; Glucose - pharmacology; Humans; Insulin - blood; Lipid Metabolism; Lipids - blood; Liver - metabolism; Liver Cirrhosis - metabolism; Liver Cirrhosis - physiopathology; Male; Middle Aged; Nitrogen - urine; Oxidation-Reduction
• ISSN: 0899-9007

Reduced thermic response after a glucose load has been reported in liver cirrhosis. To determine the mechanism and the site of this phenomenon, the effects of glucose and fructose on energy expenditure (EE) were measured in seven well-nourished cirrhotic patients and in six healthy control subjects. EE and fuel utilization were measured via indirect calorimetry for 3 h after oral glucose or fructose administration (1 g/kg body wt). After a glucose load, plasma glucose and insulin concentrations were higher in cirrhotic patients than in control subjects (p < 0.05). During the glucose trial, the cumulative incremental changes in EE over the 3-h measurement period were lower (p < 0.01) in patients 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 in the EE of control subjects (1.76 +/- 0.24 kJ.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 difference was observed between the carbohydrate oxidation in cirrhotic patients and that in control subjects, and lipid oxidation was suppressed to the same extent in both groups. We conclude that glucose-induced thermogenesis is impaired in liver cirrhosis, whereas fructose can normalize the thermic response. Because fructose is chiefly metabolized in the liver, these findings suggest that extrahepatic tissues are the site of defective thermogenesis in liver cirrhosis.