Influence of the metabolic sequelae of liver cirrhosis on nutritional intake

Abstract

Background: The liver plays a central role in ingestive behavior; alterations in metabolic signaling to the brain stem as a result of chronic liver disease could influence intake. Objective: We examined the influence of metabolic sequelae of liver disease on nutrient intake and nutritional status. Design: Nutritional status and spontaneous dietary intake were examined in 65 cirrhotic patients and 14 control subjects. The response to feeding was investigated in 14 control subjects and a subgroup of 31 cirrhotic patients. Comparisons were made between patients with primary biliary cirrhosis (PBC) and hepatocellular cirrhosis (HC). Results: Patients were nutritionally depleted. The fasting rate of lipid oxidation in the HC group was greater than in the control group (P < 0.01). In the fasting state, only HC patients were hyperinsulinemic [121.2 ± 78.5 compared with 41.3 ± 18.6 pmol/L in control subjects (P < 0.001) and 64.7 ± 15.8 pmol/L in PBC patients (P < 0.05)] and this persisted during the response to feeding. In the fed state, the magnitude of change in carbohydrate oxidation was greatest in the HC group (HC: 34.6%; control: 23.1%; PBC: 25.2%). Carbohydrate and energy intakes of the HC group were lower than in control subjects (carbohydrate: 193 ± 38.3 compared with 262 ± 48.1 g/d, P < 0.05; energy: 6.29 ± 1.40 compared with 9.0 ± 2.12 MJ/d, P < 0.05). Conclusions: Reductions in carbohydrate intake could be mediated by hyperinsulinemia and compounded by preferential uptake of carbohydrate. This may enhance gastrointestinal satiety signaling and contribute to hypophagia.