POSTPRANDIAL DE-NOVO LIPOGENESIS IN ALCOHOLIC LIVER-CIRRHOSIS - RELATIONSHIP WITH FUEL HOMEOSTASIS AND NUTRITIONAL-STATUS

The prevalence and nutritional consequences of postprandial de novo lipogenesis were evaluated in 24 stable alcoholic cirrhotic patients. Energy expenditure and the rates of nutrient oxidation were assessed by indirect calorimetry after an overnight fast and 2h after a standard meal supplying 15 kcal/kg (63kJ/kg) of body weight. Postprandially, net lipogenesis occurred in 16 patients (group L+) as shown by a respiratory quotient clearly above 1.00 (P < 0.01). The rate of lipid oxidation remained positive in 8 patients (group L-). The main mechanism involved in this metabolic pathway appeared to be a sharp postprandial hyperinsulinaemia. When compared to group L+, patient group L- showed an impaired thermic effect of food (P < 0.05), a lower rate of glucose oxidation (P < 0.05) and a mild hyperketonaemia (P < 0.05) at fasting levels. Muscular and fat masses were lower (respectively P < 0.05 and P = 0.05) and the severity of the disease as assessed by the Child-Pugh classification was more pronounced in this group (P < 0.02). The occurrence of postprandial lipogenesis in stable cirrhotic patients is related to better nutritional status. Such a metabolic pathway may explain the nutritional heterogeneity of cirrhotics and is likely to have an effect on the benefits of refeeding.