The American journal of clinical nutrition · 1999
Influence of the metabolic sequelae of liver cirrhosis on nutritional intake.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Richardson R A, Davidson H I, Hinds A, Cowan S, Rae P, Garden O J
Аннотация
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.
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.