Influence of the metabolic sequelae of liver cirrhosis on nutritional intake

Background: The liver plays a central role in ingestive behavior; alteratio ns in metabolic signaling to the brain stem as a result of chronic liver di sease 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 (PB C) and hepatocellular cirrhosis (HC). Results: Patients were nutritionally depleted. The fasting rate of lipid ox idation in the HC group was greater than in the control group (P < 0.01). I n 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 carbohyd rate 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 i n 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 hyperin sulinemia and compounded by preferential uptake of carbohydrate. This may e nhance gastrointestinal satiety signaling and contribute to hypophagia.