Insulin augmentation of glucose-stimulated insulin secretion is impaired in insulin-resistant humans.
Insulin augmentation of glucose-stimulated insulin secretion is impaired in insulin-resistant humans.
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DOI：
10.2337/db11-1067
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发表时间：
2012-02
期刊：
影响因子：
7.7
通讯作者：
Goldfine AB
中科院分区：
文献类型：
--
作者：
Halperin F;Lopez X;Manning R;Kahn CR;Kulkarni RN;Goldfine AB
2 型糖尿病 (T2D) 的特点是胰岛素抵抗和胰腺 β 细胞功能障碍，后者可能是由 β 细胞中胰岛素信号传导缺陷引起的。我们假设胰岛素抵抗者中胰岛素增强葡萄糖刺激胰岛素分泌（GSIS）的作用会减弱。为了评估胰岛素在胰岛素抵抗受试者和胰岛素敏感受试者中调节 GSIS 的效果，对 10 名糖耐量受损 (IGT) 受试者、11 名 T2D 受试者和 8 名健康对照受试者进行了两次研究。通过注射葡萄糖 80 分钟来评估胰岛素分泌反应，然后使用盐水输注（假手术）进行 4 小时钳夹，或使用 B28-Asp-胰岛素（可以在免疫学上将其与内源性胰岛素区分开）进行等血糖高胰岛素钳夹，将胰岛素浓度提高到高生理浓度。健康人预先接触胰岛素可增强 GSIS。这种效应在胰岛素抵抗人群（包括 IGT 患者和 T2D 患者）中减弱。与正常受试者相比，胰岛素在胰岛素抵抗受试者中增强葡萄糖刺激的胰岛素分泌的程度较小。这与胰岛素在体内调节人体β细胞功能的作用一致，具有治疗意义。
Type 2 diabetes (T2D) is characterized by insulin resistance and pancreatic β-cell dysfunction, the latter possibly caused by a defect in insulin signaling in β-cells. We hypothesized that insulin’s effect to potentiate glucose-stimulated insulin secretion (GSIS) would be diminished in insulin-resistant persons. To evaluate the effect of insulin to modulate GSIS in insulin-resistant compared with insulin-sensitive subjects, 10 participants with impaired glucose tolerance (IGT), 11 with T2D, and 8 healthy control subjects were studied on two occasions. The insulin secretory response was assessed by the administration of dextrose for 80 min following a 4-h clamp with either saline infusion (sham) or an isoglycemic-hyperinsulinemic clamp using B28-Asp-insulin (which can be distinguished immunologically from endogenous insulin) that raised insulin concentrations to high physiologic concentrations. Pre-exposure to insulin augmented GSIS in healthy persons. This effect was attenuated in insulin-resistant cohorts, both those with IGT and those with T2D. Insulin potentiates glucose-stimulated insulin secretion in insulin-resistant subjects to a lesser degree than in normal subjects. This is consistent with an effect of insulin to regulate β-cell function in humans in vivo with therapeutic implications.
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影响因子：
5.5
作者：
Best, CH;Haist, RE
通讯作者：
Haist, RE
影响因子：
15.9
作者：
Bernal-Mizrachi, E;Wen, W;Permutt, MA
通讯作者：
Permutt, MA
影响因子：
5.3
作者：
Assmann, Anke;Ueki, Kohjiro;Kulkarni, Rohit N.
通讯作者：
Kulkarni, Rohit N.
影响因子：
7.7
作者：
Cooperberg, Benjamin A.;Cryer, Philip E.
通讯作者：
Cryer, Philip E.
DOI：
10.1530/acta.0.0980081
发表时间：
1981-01-01
期刊：
ACTA ENDOCRINOLOGICA
影响因子：
--
作者：
DEFRONZO, RA;BINDER, C;FABER, OK
通讯作者：
FABER, OK