Riggio O, Merli M, Romiti A, Pinto G, Fanella R, Attili A F, Capocaccia L
II Cattedra di Gastroenterologia, Università di Roma La Sapienza, Italy.
JPEN J Parenter Enteral Nutr. 1992 Sep-Oct;16(5):445-50. doi: 10.1177/0148607192016005445.
The effect of meal ingestion (9 kcal/kg of body weight, 53% carbohydrate, 30% fat, 17% protein, as a liquid formula) on energy expenditure and oxidation rate of carbohydrate, fat, and protein was assessed by indirect calorimetry and urinary nitrogen excretion before and for 3 hours after eating in stable cirrhotic patients and control subjects of comparable age. Postprandial modifications of substrate and hormone levels were also studied. Compared with basal values, the mean +/- SD resting energy expenditure during the first 3 hours after meal ingestion increased similarly in cirrhotic patients (+0.32 +/- 0.12 kcal/min) and control subjects (+0.31 +/- 0.08 kcal/min). Dietary induced thermogenesis was equivalent to 10% of the energy contained in the meal in both groups. Before eating, the carbohydrate oxidation rate was lower and fat oxidation higher in cirrhotic patients than in the control subjects. After eating, glucose oxidation increased whereas fat and protein oxidation rates were reduced in both groups. As a consequence the amount of fat oxidized in the postprandial period remained higher in cirrhotic patients than in the control subjects. After meal ingestion, serum glucose levels increased whereas plasma free fatty acid and glycerol levels decreased in both groups. The substrates, however, remained significantly higher in cirrhotic patients than in control subjects, despite the higher postprandial insulin increment in the patients group, thus suggesting the presence of insulin resistance. Because the postprandial glucose oxidation rate was normal, the low insulin-mediated glucose uptake observed in cirrhotic patients seems to reflect a defect in the nonoxidative disposal of the glucose ingested.(ABSTRACT TRUNCATED AT 250 WORDS)
通过间接测热法和尿氮排泄,评估了稳定期肝硬化患者和年龄相仿的对照受试者在摄入一顿餐(9千卡/千克体重,以液体配方形式,含53%碳水化合物、30%脂肪、17%蛋白质)前后3小时内能量消耗以及碳水化合物、脂肪和蛋白质氧化率的变化。还研究了餐后底物和激素水平的改变。与基础值相比,肝硬化患者(+0.32±0.12千卡/分钟)和对照受试者(+0.31±0.08千卡/分钟)在摄入餐后的前3小时内平均静息能量消耗的增加情况相似。两组的饮食诱导产热均相当于餐中所含能量的10%。进食前,肝硬化患者的碳水化合物氧化率低于对照受试者,而脂肪氧化率则较高。进食后,两组的葡萄糖氧化均增加,而脂肪和蛋白质氧化率均降低。因此,肝硬化患者餐后氧化的脂肪量仍高于对照受试者。摄入餐后,两组的血清葡萄糖水平均升高,而血浆游离脂肪酸和甘油水平均降低。然而,尽管患者组餐后胰岛素增量较高,但肝硬化患者的底物水平仍显著高于对照受试者,这表明存在胰岛素抵抗。由于餐后葡萄糖氧化率正常,肝硬化患者中观察到的低胰岛素介导的葡萄糖摄取似乎反映了所摄入葡萄糖非氧化代谢的缺陷。(摘要截选至250词)