Franssila-Kallunki A, Rissanen A, Ekstrand A, Eriksson J, Saloranta C, Widén E, Schalin-Jäntti C, Groop L
Fourth Department of Medicine, Helsinki University Hospital, Finland.
Metabolism. 1991 Jul;40(7):689-94. doi: 10.1016/0026-0495(91)90085-b.
To examine insulin sensitivity and the relative contribution of different fuels to energy metabolism in anorexia nervosa and obesity, we measured oxidation (indirect calorimetry) of glucose, lipids, and proteins in the basal state and during an insulin clamp (+45 mU/m2.min) in 11 women with anorexia nervosa (age, 25 +/- 3 years; body mass index [BMI], 13.6 +/- 0.4 kg/m2; fat mass, 15.7% +/- 1.6%), eight obese women (age, 31 +/- 3; BMI 36.0 +/- 1.5; fat mass, 47.1% +/- 1.9%), and eight controls (age, 26 +/- 3; BMI, 21.8 +/- 0.9; fat mass, 25.7% +/- 3.6%). Expressed per lean body mass, (LBM), glucose disposal was equally reduced in anorectics (7.53 +/- 0.62 mg/kg LBM.min) and obese (6.80 +/- 1.07 mg/kg LBM.min) compared with controls (10.64 +/- 0.69 mg/kg LBM.min; P less than .01). The reduction in glucose disposal in anorectics was primarily due to a significant (P less than .01) reduction in glucose storage, while glucose oxidation was normal. In obese women, both storage and oxidation of glucose were reduced compared with controls (P less than .01). Basal energy expenditure was similar in anorectic, obese, and control subjects (20.6 +/- 1.00, 23.7 +/- 0.56, 23.2 +/- 1.36 cal/kg LBM.min, respectively). However, the contribution of glucose, lipids, and proteins to basal energy expenditure differed between anorectic (62%, 16%, 22%), obese (26%, 58%, 16%), and control (30%, 54%, 16%) subjects (P less than .05 v all). In conclusion, in anorexia nervosa, insulin stimulates glucose oxidation more than storage. In obesity, both components of insulin-stimulated glucose metabolism are impaired.(ABSTRACT TRUNCATED AT 250 WORDS)
为研究神经性厌食症和肥胖症患者的胰岛素敏感性以及不同燃料对能量代谢的相对贡献，我们测量了11名神经性厌食症女性（年龄25±3岁；体重指数[BMI]13.6±0.4kg/m²；脂肪量15.7%±1.6%）、8名肥胖女性（年龄31±3岁；BMI 36.0±1.5；脂肪量47.1%±1.9%）和8名对照者（年龄26±3岁；BMI 21.8±0.9；脂肪量25.7%±3.6%）在基础状态下以及胰岛素钳夹试验（+45mU/m²·min）期间葡萄糖、脂质和蛋白质的氧化情况（间接测热法）。以瘦体重（LBM）表示，与对照组（10.64±0.69mg/kg LBM·min）相比，神经性厌食症患者（7.53±0.62mg/kg LBM·min）和肥胖者（6.80±1.07mg/kg LBM·min）的葡萄糖处置均同等程度降低（P<0.01）。神经性厌食症患者葡萄糖处置的降低主要是由于葡萄糖储存显著减少（P<0.01），而葡萄糖氧化正常。在肥胖女性中，与对照组相比，葡萄糖的储存和氧化均降低（P<0.01）。神经性厌食症患者、肥胖者和对照者的基础能量消耗相似（分别为20.6±1.00、23.7±0.56、23.2±1.36cal/kg LBM·min）。然而，神经性厌食症患者（62%、16%、22%）、肥胖者（26%、58%、16%）和对照者（30%、54%、16%）之间葡萄糖、脂质和蛋白质对基础能量消耗的贡献有所不同（P<0.05，与所有组相比）。总之，在神经性厌食症中，胰岛素刺激葡萄糖氧化多于储存。在肥胖症中，胰岛素刺激的葡萄糖代谢的两个组成部分均受损。（摘要截断于250字）
