ENERGY-EXPENDITURE AND SUBSTRATE METABOLISM AFTER ORAL FRUCTOSE IN PATIENTS WITH CIRRHOSIS

There is little information on the metabolic response to ingested fruc tose in patients with cirrhosis. Glucose kinetics, plasma lipid and bl ood lactate levels, whole body substrate oxidation rates and energy ex penditure were measured following ingestion of 75 g fructose, in 8 cir rhotic patients and 6 controls. Fasting plasma glucose levels and rate s of glucose appearance (Ra) and disappearance (Rd) were similar. The basal rate of lipolysis was higher in cirrhotic patients (P < 0.05), b ut whole body lipid and carbohydrate oxidation rates and energy expend iture were similar. After fructose ingestion, plasma fructose levels w ere much higher in cirrhotic patients (P < 0.001) and the incremental area under the plasma glucose curve was twice that of controls (P < 0. 05). The increase in glucose in patients with cirrhosis was due to an increase in glucose Pa and an initial reduction in glucose Rd. Plasma non-esterified fatty acid levels fell to similar low levels in both gr oups. Glycerol levels fell in controls (P < 0.05) but not in cirrhotic patients. Blood lactate levels, fasting and after oral fructose, were similar in cirrhotics and controls. The time course of suppression of lipid oxidation and stimulation of carbohydrate oxidation was more cl osely related to fructose levels than to serum fatty acid levels in bo th groups. The percent suppression and total quantity of lipid oxidize d in 4 h after fructose were not significantly different, but the supp ressed lipid oxidation rates and elevated carbohydrate oxidation rates were sustained for longer in the cirrhotics. The data suggest that fr uctose uptake and metabolism inhibits oxidation of intracellular lipid . There was a smaller increase in energy expenditure after fructose in cirrhotics (P < 0.001), but normal overall storage of fructose; the l ikely explanation is reduced first pass hepatic fructose uptake in cir rhotics making more fructose available to the periphery for incorporat ion into muscle glycogen. The energy cost of storing fructose as muscl e glycogen is less than that of storing it as liver glycogen. Preferen tial incorporation of fructose carbon into muscle glycogen, with lower rates of hepatic glycogen and triglyceride synthesis, would therefore result in less energy expenditure after a fructose load in cirrhotics .