Knop Filip K, Vilsbøll Tina, Højberg Patricia V, Larsen Steen, Madsbad Sten, Vølund Aage, Holst Jens J, Krarup Thure
Department of Internal Medicine F, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark.
Diabetes. 2007 Aug;56(8):1951-9. doi: 10.2337/db07-0100. Epub 2007 May 18.
We aimed to investigate whether the reduced incretin effect observed in patients with type 2 diabetes is a primary event in the pathogenesis of type 2 diabetes or a consequence of the diabetic state. Eight patients with chronic pancreatitis and secondary diabetes (A1C mean [range] of 6.9% [6.2-8.0]), eight patients with chronic pancreatitis and normal glucose tolerance (NGT; 5.3 [4.9-5.7]), eight patients with type 2 diabetes (6.9 [6.2-8.0]); and eight healthy subjects (5.5 [5.1-5.8]) were studied. Blood was sampled over 4 h on 2 separate days after a 50-g oral glucose load and an isoglycemic intravenous glucose infusion, respectively. The incretin effect (100% x [beta-cell secretory response to oral glucose tolerance test - intravenous beta-cell secretory response]/beta-cell secretory response to oral glucose tolerance test) was significantly (P < 0.05) reduced (means +/- SE) in patients with chronic pancreatitis and secondary diabetes (31 +/- 4%) compared with patients with chronic pancreatitis and NGT (68 +/- 3) and healthy subjects (60 +/- 4), respectively. In the type 2 diabetes group, the incretin effect amounted to 36 +/- 6%, significantly (P < 0.05) lower than in chronic pancreatitis patients with NGT and in healthy subjects, respectively. These results suggest that the reduced incretin effect is not a primary event in the development of type 2 diabetes, but rather a consequence of the diabetic state.
我们旨在研究2型糖尿病患者中观察到的肠促胰岛素效应降低是2型糖尿病发病机制中的原发性事件还是糖尿病状态的结果。研究了8例慢性胰腺炎继发糖尿病患者（糖化血红蛋白平均值[范围]为6.9%[6.2 - 8.0]）、8例慢性胰腺炎且糖耐量正常（NGT；5.3[4.9 - 5.7]）的患者、8例2型糖尿病患者（6.9[6.2 - 8.0]）以及8例健康受试者（5.5[5.1 - 5.8]）。分别在给予50克口服葡萄糖负荷和等血糖静脉输注葡萄糖后，于2个不同日期的4小时内采集血液样本。与慢性胰腺炎且糖耐量正常的患者（68±3）和健康受试者（60±4）相比，慢性胰腺炎继发糖尿病患者的肠促胰岛素效应（100%×[口服葡萄糖耐量试验的β细胞分泌反应 - 静脉β细胞分泌反应]/口服葡萄糖耐量试验的β细胞分泌反应）显著降低（P<0.05）（平均值±标准误），为31±4%。在2型糖尿病组中，肠促胰岛素效应为36±6%，分别显著低于慢性胰腺炎且糖耐量正常的患者和健康受试者（P<0.05）。这些结果表明，肠促胰岛素效应降低不是2型糖尿病发生发展的原发性事件，而是糖尿病状态的结果。
