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目的研究肥胖和非肥胖糖耐量受损(IGT)患者的胰岛素敏感性和β细胞1相胰岛素分泌功能,以探讨在IGT患者中肥胖对胰岛素抵抗和1相胰岛素分泌的影响。方法共有99位受试者(包括正常对照者32名,肥胖IGT44例,非肥胖IGT23例)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(采血样12次)的Bergman微小模型技术结合静脉葡萄糖耐量试验(FSIGTT)。胰岛素抵抗由FSIGTT中胰岛素敏感性指数(SI)加以评估,而OGTT中糖负荷后30 min胰岛素增值与血糖增值之比值[ΔI30/ΔG30=(I30 min-I0 min) /(G30 min-G0 min)]和FSIGTT中急性胰岛素分泌反应(AIRg)则用以评价胰岛β细胞分泌功能。处理指数(DI =AIRg×SI)用于评价AIRg是否代偿机体的胰岛素抵抗。结果与正常对照组[(7.52±10.89)×10-4]相比,二组IGT患者之SI明显降低,而肥胖IGT组的SI[(1.72±1.11)×10-4]较非肥胖组[(3.15±1.49)×10-4]更低(均P<0.01); AIRg和ΔI30/ΔG30在正常组(412±191,14.45±8.47)和肥胖IGT组(378±235,17.02±11.30)之间差异无统计学意义,但均大于非肥胖组(196±160,8.93±6.69,均P<0.01);与正常组(2 851±1 180)相比,DI指数在二组IGT显著降低(595±485,584±517),但后二组间此值差异无统计学意义。SI与2 h胰岛素、体重指数、尿酸和胆固醇呈显著的负相关性(校正r2=0.603,P<0.01);而AIRg与ΔI30/ΔG30显著正相关,与空腹血糖负相关(校正r2=0.479,P<0.01)。结论IGT患者存在胰岛素抵抗和β细胞功能异常。与非肥胖IGT患者相比,肥胖IGT患者胰岛素抵抗程度更为严重,但胰岛β细胞胰岛素1相分泌相对充分。
Objective To investigate insulin sensitivity and β-cell 1-phase insulin secretion in obese and non-obese patients with impaired glucose tolerance (IGT) to investigate the effects of obesity on insulin resistance and 1-phase insulin secretion in IGT patients. Methods A total of 99 subjects (32 normal controls, 44 obese IGTs and 23 non-obese IGT patients) received Bergman’s oral 75 g glucose tolerance test (OGTT) and insulin-modified reduced sample number (12 blood samples) Micro-model technique combined with intravenous glucose tolerance test (FSIGTT). Insulin resistance was assessed by the insulin sensitivity index (FSI) in FSIGTT, and the ratio of insulin increase to glycemic excretion at 30 min after glucose loading in OGTT [ΔI30 / ΔG30 = (I30 min -I0 min) / (G30 min -G0 min) ] And acute insulin secretion response (AIRg) in FSIGTT were used to assess pancreatic β-cell secretory function. The treatment index (DI = AIRg × SI) was used to evaluate whether AIRg compensates for the body’s insulin resistance. Results Compared with the normal control group [(7.52 ± 10.89) × 10-4], SI in two IGT patients was significantly lower than that in the non-obese group [(1.72 ± 1.11) × 10-4] (3.15 ± 1.49) × 10-4] (all P <0.01); AIRg and ΔI30 / ΔG30 were significantly lower in the normal group (412 ± 191,14.45 ± 8.47) and obese IGT group (378 ± 235,17.02 ± 11.30) (P <0.01). Compared with the normal group (2 851 ± 1 180), the DI index in the two groups was significantly lower than that in the non-obese group (196 ± 160,8.93 ± 6.69, P <0.01) 595 ± 485,584 ± 517), but the difference between the latter two groups was not statistically significant. SI was negatively correlated with 2 h insulin, body mass index, uric acid and cholesterol (r2 = 0.603, P <0.01), while AIRg was positively correlated with ΔI30 / ΔG30 and negatively correlated with fasting glucose (r2 = 0.479, P <0.01). Conclusion IGT patients have insulin resistance and β-cell dysfunction. Compared with non-obese patients with IGT, IGT patients with obesity more severe insulin resistance, but pancreatic β-cell insulin secretion phase 1 is relatively adequate.