Defective insulin secretion in NIDDM: integral part of a multiplier hypothesis.
Defective insulin secretion in NIDDM: integral part of a multiplier hypothesis.
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NIDDM 中的胰岛素分泌缺陷：乘数假设的组成部分。
DOI：
10.1002/jcb.240480302
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发表时间：
1992
影响因子：
4
通讯作者：
Robertson,RP
中科院分区：
文献类型：
--
作者：
Robertson,RP
非胰岛素依赖型糖尿病（NIDDM）的特征在于胰岛β细胞对葡萄糖识别的特异性缺陷。这与患有胰岛素依赖型糖尿病（IDDM）的患者明显不同，所述患者经历胰岛β细胞死亡并且不再具有合成、储存和释放胰岛素的能力。NIDDM患者葡萄糖诱导的胰岛素第一时相反应缺陷可通过外源性胰岛素治疗和其他药物治疗部分恢复。这些观察结果为胰腺β细胞葡萄糖脱敏作为NIDDM胰岛素分泌异常发病机制中重要的继发性缺陷的理论提供了力量。然而，尽管胰岛素分泌缺陷是NIDDM发病机制的重要组成部分，但其本身是不够的。需要一种倍增效应，涉及组织对胰岛素作用的抵抗和胰岛素分泌缺陷之间的相互作用，其产物是NIDDM综合征。
Non‐insulin dependent diabetes mellitus (NIDDM) is characterized by a specific defect in glucose recognition by the pancreatic islet beta cell. This is in clear distinction to patients with insulin dependent diabetes mellitus (IDDM) who undergo pancreatic islet beta cell death and no longer have the ability to synthesize, store, and release insulin. Defective glucose‐induced first phase insulin responses in patients with NIDDM can be partially restored by exogenous insulin treatment and by other pharmacologic therapy. These observations provide strength for the theory of glucose desensitization of the pancreatic beta cell as an important secondary defect in the pathogenesis of abnormal insulin secretion in NIDDM. However, even though defective insulin secretion is an essential part of the pathogenesis of NIDDM, in itself it is not sufficient. A multiplicative effect is required involving interaction between tissue resistance to insulin action and defective insulin secretion whose product is the syndrome of NIDDM.