Kahn S E, Prigeon R L, McCulloch D K, Boyko E J, Bergman R N, Schwartz M W, Neifing J L, Ward W K, Beard J C, Palmer J P
Department of Medicine, University of Washington, Seattle.
Diabetes. 1994 Apr;43(4):587-92. doi: 10.2337/diab.43.4.587.
Glucose disposal occurs by both insulin-independent and insulin-dependent mechanisms, the latter being determined by the interaction of insulin sensitivity and insulin secretion. To determine the role of insulin-independent and insulin-dependent factors in glucose tolerance, we performed intravenous glucose tolerance tests on 93 young healthy subjects (55 male, 38 female; 18-44 years of age; body mass index, 19.5-52.2 kg/m2). From these tests, we determined glucose tolerance as the glucose disappearance constant (Kg), calculated beta-cell function as the incremental insulin response to glucose for 19 min after an intravenous glucose bolus (IIR0-19), and derived an insulin sensitivity index (SI) and glucose effectiveness at basal insulin (SG) using the minimal model of glucose kinetics. To eliminate the effect of basal insulin on SG and estimate insulin-independent glucose uptake, we calculated glucose effectiveness at zero insulin (GEZI = SG - [SI x basal insulin]). Insulin-dependent glucose uptake was estimated as SI x IIR0-19, because the relationship between SI and beta-cell function has been shown to be hyperbolic. Using linear regression to determine the influence of these factors on glucose tolerance, we found that GEZI was significantly related to Kg (r = 0.70; P < 0.0001), suggesting a major contribution of insulin-independent glucose uptake to glucose disappearance. As expected, SI x IIR0-19 also correlated well with Kg (r = 0.74; P < 0.0001), confirming the importance of insulin-dependent glucose uptake to glucose tolerance. Although IIR0-19 alone correlated with Kg (r = 0.35; P = 0.0005), SI did not (r = 0.18; P > 0.08).(ABSTRACT TRUNCATED AT 250 WORDS)
葡萄糖的处置通过胰岛素非依赖和胰岛素依赖两种机制进行，后者由胰岛素敏感性和胰岛素分泌的相互作用决定。为了确定胰岛素非依赖和胰岛素依赖因素在葡萄糖耐量中的作用，我们对93名年轻健康受试者（55名男性，38名女性；年龄18 - 44岁；体重指数19.5 - 52.2 kg/m²）进行了静脉葡萄糖耐量试验。通过这些试验，我们将葡萄糖耐量确定为葡萄糖消失常数（Kg），将β细胞功能计算为静脉注射葡萄糖推注后19分钟内对葡萄糖的胰岛素增量反应（IIR0 - 19），并使用葡萄糖动力学的最小模型得出胰岛素敏感性指数（SI）和基础胰岛素水平下的葡萄糖效能（SG）。为了消除基础胰岛素对SG的影响并估计胰岛素非依赖的葡萄糖摄取，我们计算了零胰岛素水平下的葡萄糖效能（GEZI = SG - [SI×基础胰岛素]）。胰岛素依赖的葡萄糖摄取估计为SI×IIR0 - 19，因为SI与β细胞功能之间的关系已被证明是双曲线关系。使用线性回归来确定这些因素对葡萄糖耐量的影响，我们发现GEZI与Kg显著相关（r = 0.70；P < 0.0001），表明胰岛素非依赖的葡萄糖摄取对葡萄糖消失有主要贡献。正如预期的那样，SI×IIR0 - 19也与Kg密切相关（r = 0.74；P < 0.0001），证实了胰岛素依赖的葡萄糖摄取对葡萄糖耐量的重要性。尽管单独的IIR0 - 19与Kg相关（r = 0.35；P = 0.0005），但SI与Kg不相关（r = 0.18；P > 0.08）。（摘要截断于250字）
