DIFFERENTIAL-EFFECTS OF INSULIN RESISTANCE ON LEUCINE AND GLUCOSE KINETICS IN OBESITY
DIFFERENTIAL-EFFECTS OF INSULIN RESISTANCE ON LEUCINE AND GLUCOSE KINETICS IN OBESITY
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DOI：
10.1016/0026-0495(91)90192-y
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发表时间：
1991-01-01
影响因子：
9.8
通讯作者：
WURTMAN, RJ
中科院分区：
文献类型：
--
作者：
CABALLERO, B;WURTMAN, RJ
研究了胰岛素抵抗对肥胖非糖尿病女性（体重指数[BMI]为（32.8±2））和瘦肉对照组葡萄糖和氨基酸代谢的影响。通过持续注入d-[6,6- 2h2]葡萄糖和l-[1-13C]亮氨酸，同时测量吸收后状态和正糖高胰岛素血症期间葡萄糖处置率、肝脏葡萄糖生成、亮氨酸碳通量和氧化。每名受试者分别在10和40 μU (m2·min)−1的输注速率下参加两次胰岛素钳夹研究，血浆胰岛素水平分别为20 ~ 25和70 ~ 80 μU/mL。无脂质量（FFM）由水下称重测量计算。胰岛素介导的葡萄糖处置率在肥胖组明显较慢：在10 mu胰岛素夹夹期间，胰岛素介导的葡萄糖处置率为2.05±0.05，对照组为3.84±0.18 mg (kg·min)−1；在40 mu胰岛素夹夹期间，胰岛素介导的葡萄糖处置率为3.80±0.23，对照组为9.16±0.47 mg (kg·min)−1。胰岛素引起的支链氨基酸血浆水平下降在肥胖组也明显减弱。基线亮氨酸通量在瘦人和肥胖者中相似（分别为78±3和71±2 μmol (kg·h)−1），其对胰岛素输注的响应下降也相似（在10 μmol /m2夹夹期间分别为8%和10%，在40 μmol /m2夹夹期间分别为17%和18%）。基础亮氨酸碳氧化（来自[13C]亮氨酸和[13C]α酮异己酸[α-KIC]血浆富集）在瘦人和肥胖者中也相似，并且在胰岛素输注时没有显著变化。两组瘦体重与血浆支链氨基酸水平之间存在显著相关（R2= 0.93）。这些结果表明，肥胖中常见的血浆支链氨基酸水平升高并不一定与胰岛素介导的氨基酸通量受损有关，其他因素，如身体成分，也可能是肥胖高氨基酸酸血症的决定因素。
The effects of insulin resistance on glucose and amino acid metabolism were studied in obese nondiabetic women (body mass index [BMI], (32.8 ± 2) and in lean controls. Glucose disposal rate, hepatic glucose production, and leucine carbon flux and oxidation were simultaneously measured during the postabsorptive state and during euglycemic hyperinsulinemia, by means of primed, constant infusions ofd-[6,6-2H2]glucose andl-[1-13C]leucine. Each subject participated in two insulin clamp studies on separate days, at infusion rates of 10 and 40 mU (m2· min)−1, producing plasma insulin levels of 20 to 25 and 70 to 80 μU/mL, respectively. Fat-free mass (FFM) was calculated from underwater weighing measurements. Insulin-mediated glucose disposal rate was significantly slower in the obese group: 2.05 ± 0.05 versus 3.84 ± 0.18 mg (kg · min)−1in controls during the 10-mU insulin clamp, and 3.80 ± 0.23 versus 9.16 ± 0.47 mg (kg · min)−1during the 40-mU clamp. The insulin-induced decrease in plasma levels of branched chain amino acids was also significantly blunted in the obese group. Baseline leucine flux was similar in lean and obese subjects (78 ± 3 and 71 ± 2 μmol (kg · h)−1, respectively), and its decline in response to insulin infusion was also comparable (8% and 10% during the 10-mU/m2clamp, and of 17% and 18% during the 40-mU/m2clamp in lean and obese, respectively). Basal leucine carbon oxidation (from [13C]leucine and [13C]αketoisocaproate [α-KIC] plasma enrichments) was also similar in lean and obese, and did not change significantly with insulin infusion. A significant correlation (R2= .93) was found in both groups between lean body mass and plasma levels of branched chain amino acids. These results indicate that the elevation in plasma branched chain amino acid levels commonly observed in obesity is not necessarily associated with an impaired insulin-mediated amino acid flux, and that other factors, such as body composition, may be also determinants of the hyperaminoacidemia of obesity.