Reduced incretin effect in type 2 diabetes - Cause or consequence of the diabetic state?
Reduced incretin effect in type 2 diabetes - Cause or consequence of the diabetic state?
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DOI：
10.2337/db07-0100
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发表时间：
2007-08-01
期刊：
影响因子：
7.7
通讯作者：
Krarup, Thure
中科院分区：
文献类型：
--
作者：
Knop, Filip K.;Vilsboll, Tina;Krarup, Thure
我们的目的是调查在2型糖尿病患者中观察到的胰岛素降低效应是2型糖尿病发病机制中的主要事件还是糖尿病状态的结果。研究对象包括8例慢性胰腺炎和继发性糖尿病患者(A1C平均值6.9%[6.2-8.0])、8例慢性胰腺炎和正常糖耐量(NGT；5.3[4.9-5.7])、8例2型糖尿病患者(6.9[6.2-8.0])和8例健康人(5.5[5.1-5.8])。分别在口服50g葡萄糖负荷和静脉输注等血糖葡萄糖后两天，在4h内采集血液样本。胰岛素效应(100%x[β细胞对口服葡萄糖耐量试验的分泌反应-静脉注射β细胞。慢性胰腺炎和继发性糖尿病患者(31+/-4%)显著低于慢性胰腺炎和NGT患者(68.3%)和正常人(60.4%)(P<；0.05)。在2型糖尿病组中，INT效应达36+/-6%，显著低于慢性胰腺炎合并NGT组和健康对照组(P<；0.05)。这些结果表明，胰岛素效应的降低不是2型糖尿病发展的主要事件，而是糖尿病状态的结果。
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.