糖耐量不同的代谢综合征患者胰岛素抵抗和胰岛β细胞1相胰岛素分泌功能的研究

A study of the degrees of insulin resistance and first-phase insulin secretion of β-cells in metabolic syndrome patients with different glucose tolerance

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。

Objective To explore the insulin resistance and first-phase insulin secretion of β-cells in normal persons, obese persons with normal glucose tolerance,obese persons with impaired glucose tolerance (IGT) and obese persons with type 2 diabetes (T2DM). Methods 75 g oral glucose tolerance test (OGTT) and Bergman's minimal model method of frequently sampled intravenous glucose tolerance test (FSIGTT) with reduced sample number (n=12) were performed on a total of 151 subjects, 29 normal controls (control group), 44 obese persons with normal glucose tolerance (obesity group), 36 obese persons with IGT (IGT group), and 42 T2DMT patients (T2DM group) to determine the acute insulin response to glucose (AIRg), insulin sensitivity index (S I), and glucose effectiveness (S G). The disposition index (DI, AIRg X S I) was calculated to determine whether AIRg was adequate to compensate for insulin resistance. Results The S I value of the control group was significantly higher than those of the obesity,IGT, and T2DM groups (all P<0.01), without significant difference among the latter three groups. The S G value of the control group was not significantly different from that of the obesity group, but significantly higher than those of the IGT and T2DM groups (both P<0.01),without significant difference any 2 groups from the latter two groups. The AIRg of the normal group was similar to that of the IGT group (2.61 mU·L -1·min -1±0.13 mU·L -1·min -1 vs 2.56 mU·L -1·min -1±0.25 mU·L -1·min -1), and significantly lower than that of the obesity group (3.02 mU·L -1·min -1 ±0.27 mU·L -1·min -1, P<0.01) and higher than that of the T2DM group (1.54 mU·L -1·min -1±0.55 mU·L -1·min -1, P<0.01). The value of DI was gradually decreased from the sequence of the groups of control, obesity, IGT, and T2DM (3.16±0.31?2.65±0.50?1.67±0.54), with significant differences between any two groups (all P<0.01). Multiple regression analyses with S I and AIRg as dependent variables showed that S I was negatively correlated with BMI, 2 h glucose level in OGTT, 2 h insulin, triglyceride, and cholesterol (r2=0.589, P<0.001), and AIRg was positively correlated with BMI, S G, fasting insulin, and 2 h insulin level and negatively correlated with 2 h glucose, and age (r2=0.515, P<0.001).Conclusion Obese patients with different glucose tolerance have similar degrees of insulin resistance. Acute insulin response is increased in obesity group to compensate for the insulin resistance. Although the acute insulin response in the IGT group is similar to that in the control group, however, the compensation of islet β cells in the IGT group is significantly decreased as compared with that in the obesity group, leading to glucose intolerance. There is a severe deficiency of acute insulin response to glucose in T2DM group.