Gniuli D, Liverani E, Capristo E, Greco A V, Mingrone G
Department of Metabolic Disease, Catholic University, School of Medicine, Rome, Italy.
Metabolism. 2001 Aug;50(8):876-81. doi: 10.1053/meta.2001.24915.
Only few studies have specifically investigated diet-induced thermogenesis in anorexia nervosa. Twenty women, 10 anorectics (body mass index [BMI] = 14.98 +/- 1.02 kg/m(2)) and 10 controls (BMI = 22.53 +/- 0.75 kg/m(2)) were studied. Body composition was evaluated by isotopic dilution. Respiratory gas exchange was measured by indirect calorimetry. An oral glucose load (75 g) was administered to the anorectics (A) and the controls (CA). The controls underwent a second load (CB) with a higher glucose amount (1.85 +/- 0.11 g/kg body weight [BW]) to compare with the load taken by anorectics. Glucose-induced thermogenesis (GIT) was computed for 300 minutes following the load as the percent increase of energy expenditure (EE) above resting-EE (REE). Serum glucose levels were lower in anorectic patients both in fasting (3.46 +/- 0.66 v 5.23 +/- 0.23 in CA, P <.01 v 5.32 +/- 0.34 mmol in CB, P <.01) and in the postprandial state (glucose area under the curve [AUC] 175.51 +/- 6.40 v 289.80 +/- 7.30 in CA, P <.01 v 324.65 mmol in CB, P <.001); insulin AUC was lower, 1,926 +/- 452 versus 41,148 +/- 2,071 in CA, P <.0001 versus 60,765.5 pmol in CB, P <.0001. REE, normalized by fat-free mass (FFM), was similar between groups. GIT was lower in anorectics (3.58 +/- 1.20 v 5.45 +/- 1.83 in CA, P <.05 v 9.09% +/- 1.05% in CB, P <.01). Glucose oxidation was higher in anorectics than in CA (689.44 +/- 72.22 v 333.32 +/- 32.98 micromol/L/min, P <.001), but similar to CB. Lipid oxidation become negative after 30 minutes in anorectics (postprandial lipid oxidation = -93.58 +/- 39.86 v 370.61 +/- 21.73 in CA, P <.0001 v 119.01 +/- 12.32 micromol/L/300 min in CB, P <.0001). Anorectic patients displayed a low REE and GIT. Carbohydrate oxidation was similar between groups; lipid oxidation was extremely reduced. An increased protein catabolism was observed.
仅有少数研究专门调查了神经性厌食症中饮食诱导的产热情况。对20名女性进行了研究，其中10名厌食症患者（体重指数[BMI]=14.98±1.02kg/m²）和10名对照者（BMI=22.53±0.75kg/m²）。通过同位素稀释法评估身体成分。通过间接测热法测量呼吸气体交换。给厌食症患者（A组）和对照者（CA组）口服葡萄糖负荷（75g）。对照者接受第二次更高葡萄糖量（1.85±0.11g/kg体重[BW]）的负荷（CB组），以与厌食症患者所接受的负荷进行比较。负荷后300分钟内计算葡萄糖诱导的产热（GIT），即能量消耗（EE）高于静息能量消耗（REE）的百分比增加量。厌食症患者的空腹血清葡萄糖水平较低（CA组为3.46±0.66，而CA组为5.23±0.23，P<0.01；CB组为5.32±0.34mmol，P<0.01），餐后状态下也是如此（曲线下葡萄糖面积[AUC]：CA组为175.51±6.40，而CA组为289.80±7.30，P<0.01；CB组为324.65mmol，P<0.001）；胰岛素AUC较低，CA组为1,926±452，而CA组为41,148±2,071，P<0.0001；CB组为60,765.5pmol，P<0.0001。按去脂体重（FFM）标准化后的REE在两组之间相似。厌食症患者的GIT较低（CA组为3.58±1.20，P<0.05；CB组为9.09%±1.05%，P<0.01）。厌食症患者的葡萄糖氧化高于CA组（689.44±72.22对333.32±32.98微摩尔/升/分钟，P<0.001），但与CB组相似。厌食症患者在30分钟后脂质氧化变为负值（餐后脂质氧化=-93.58±39.86对CA组的370.61±21.73，P<0.0001；CB组为119.01±12.32微摩尔/升/300分钟，P<0.0001）。厌食症患者表现出低REE和GIT。碳水化合物氧化在两组之间相似；脂质氧化极度减少。观察到蛋白质分解代谢增加。
