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目的 研究正常人、糖耐量正常肥胖 (肥胖 )、肥胖伴糖耐量减退 (IGT)和肥胖伴 2型糖尿病 (T2DM)患者的胰岛素抵抗和胰岛 β细胞 1相胰岛素分泌功能。 方法 15 1位受试者接受了口服 75 g葡萄糖耐量试验 (OGTT)和胰岛素改良的减少样本数 (n =12 )的Bergman微小模型技术 ,结合多样本静脉葡萄糖耐量试验 (FSIGTT) ,前者用以诊断糖耐量有无异常 ,后者用以测定机体的胰岛素敏感性指数 (SI)、葡萄糖自身代谢效能 (SG)和机体对FSIGTT中葡萄糖负荷后的胰岛素分泌反应(AIRg) ,应用处理指数 (DI =AIRg×SI)评价AIRg是否足以代偿机体的胰岛素抵抗。 结果 正常组的SI 显著高于肥胖、IGT和T2DM组 (P <0 0 1) ,后 3组间差异无显著意义。正常组与肥胖组的SG无明显差异 ,但显著大于IGT和T2DM组 (P <0 0 1) ,后 2组间差异无显著意义 ;正常组与IGT组的AIRg(2 6 1mU·L-1·min-1± 0 13mU·L-1·min-1vs 2 5 6mU·L-1·min-1± 0 2 5mU·L-1·min-1)差异无显著意义 ,但小于肥胖组 (3 0 2mU·L-1·min-1± 0 2 7mU·L-1·min-1,P <0 0 1)而大于T2DM组 (1 5 4mU·L-1·min-1± 0 5 5mU·L-1·min-1,P <0 0 1) ;DI值则由正常组 (3 4 4± 0 17)向肥胖组、IGT和T2DM组依次降低 (3 16± 0 31、2 6 5± 0 5 0、1
Objective To investigate insulin resistance and pancreatic β-cell 1-phase insulin secretion in normal subjects, patients with normal glucose tolerance (obesity), obesity with impaired glucose tolerance (IGT) and obesity with type 2 diabetes (T2DM). Method 15 One participant received the Bergman mini-model technique for oral 75 g glucose tolerance test (OGTT) and insulin-modified reduced sample size (n = 12), in combination with a multi-sample intravenous glucose tolerance test (FSIGTT) The latter was used to determine the body’s insulin sensitivity index (SI), glucose self-metabolism (SG) and the body’s insulin secretion response (AIRg) after glucose loading in FSIGTT, and the application treatment index = AIRg × SI) To evaluate whether AIRg is sufficient to compensate for the body’s insulin resistance. Results The SI of the normal group was significantly higher than that of the obese, IGT and T2DM groups (P <0.01). There was no significant difference in the latter three groups. There was no significant difference in SG between normal group and obesity group, but significantly higher than IGT group and T2DM group (P <0.01), there was no significant difference between the latter two groups. AIRg (2 6 1mU · L-1 · Min-1 ± 0 13mU · L-1 · min-1vs 2 5 6mU · L-1 · min-1 ± 0 2 5mU · L-1 · min-1) was no significant difference, (P <0.01), which was significantly higher than that of T2DM group (154mU · L-1 · min-1 ± 055mU · L-1 · min-1 ± 0 2 7mU · L-1 · min- L-1 · min-1, P <0.01). DI value decreased from 34 34 ± 0 17 to obesity group, IGT and T2DM groups (3 16 ± 0 31 and 2 65 ± 0 5 0,1