Impairment of early insulin response after glucose load, rather than insulin resistance, is responsible for postprandial hyperglycemia seen in obese type 2 diabetes: Assessment using nateglinide, a new insulin secretagogue
Impairment of early insulin response after glucose load, rather than insulin resistance, is responsible for postprandial hyperglycemia seen in obese type 2 diabetes: Assessment using nateglinide, a new insulin secretagogue
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DOI：
10.1507/endocrj.47.639
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发表时间：
2000-10-01
影响因子：
2
通讯作者：
Kawamori, R
中科院分区：
文献类型：
--
作者：
Uchino, H;Niwa, M;Kawamori, R
作为 2 型糖尿病表型的胰岛素分泌模式是响应餐后血糖升高而快速、脉动地分泌胰岛素的障碍。通过使用新开发的胰岛素促分泌剂那格列奈，首次在患有 2 型糖尿病的肥胖患者中建立了口服葡萄糖负荷后内源性快速胰岛素分泌恢复的方法。清楚地证明，使用那格列奈后，血清胰岛素水平迅速升高，并且在 180 分钟内胰岛素分泌量相同的情况下，血糖反应曲线几乎趋于正常化。因此，肥胖2型糖尿病患者餐后血糖反应的原因是口服葡萄糖负荷后血糖升高时缺乏快速、脉动的胰岛素分泌，而不是胰岛素抵抗。
The insulin secretory pattern as a phenotype of type 2 diabetes is an impairment in the rapid, pulsatile secretion of insulin in response to a rise in blood glucose after meal-intake. The restoration of endogenous rapid insulin secretion after oral glucose load was established for the first time by using nateglinide, which is a newly developed insulin secretagogue, in obese patients with type 2 diabetes mellitus. It was clearly demonstrated that with nateglinide, serum insulin levels were quickly raised, and glycemic response curves were almost normalized with the same amount of insulin secretion during 180 min. Therefore, the lack of rapid, pulsatile secretion of insulin in response to glycemic rise after oral glucose load, rather than insulin resistance, is responsible for postprandial glycemic response in obese type 2 diabetes patients.