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  • Title: Energy expenditure and substrate metabolism after oral fructose in patients with cirrhosis.
    Author: Kruszynska YT, Meyer-Alber A, Wollen N, McIntyre N.
    Journal: J Hepatol; 1993 Sep; 19(2):241-51. PubMed ID: 8301057.
    Abstract:
    There is little information on the metabolic response to ingested fructose in patients with cirrhosis. Glucose kinetics, plasma lipid and blood lactate levels, whole body substrate oxidation rates and energy expenditure were measured following ingestion of 75 g fructose, in 8 cirrhotic patients and 6 controls. Fasting plasma glucose levels and rates of glucose appearance (Ra) and disappearance (Rd) were similar. The basal rate of lipolysis was higher in cirrhotic patients (P < 0.05), but whole body lipid and carbohydrate oxidation rates and energy expenditure were similar. After fructose ingestion, plasma fructose levels were 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 Ra and an initial reduction in glucose Rd. Plasma non-esterified fatty acid levels fell to similar low levels in both groups. 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 closely related to fructose levels than to serum fatty acid levels in both groups. The percent suppression and total quantity of lipid oxidized in 4 h after fructose were not significantly different, but the suppressed lipid oxidation rates and elevated carbohydrate oxidation rates were sustained for longer in the cirrhotics. The data suggest that fructose 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 likely explanation is reduced first pass hepatic fructose uptake in cirrhotics making more fructose available to the periphery for incorporation into muscle glycogen. The energy cost of storing fructose as muscle glycogen is less than that of storing it as liver glycogen. Preferential 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.
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