论文部分内容阅读
T2DM根据IR和胰岛β细胞功能障碍进行分类,后者可能是胰岛β细胞胰岛素信号缺陷引起的。为评估IR人群较之胰岛素敏感人群在胰岛素调节葡萄糖刺激的胰岛素分泌(GSIS)方面的作用,美国研究者对10例IGT患者,11例T2DM患者以及8名健康对照者进行了研究。输注生理盐水或采用B28-Asp-胰岛素进行正常血糖-高血胰岛素钳夹试验4h后给予右旋糖80min评估胰岛素分泌反应。结果发现,之前暴露于胰岛素的健康人群GSIS增加。这一作用在有IR的人群中减弱,IGT和
T2DM is classified according to IR and pancreatic β-cell dysfunction, which may be caused by a deficiency of islet β-cell insulin signaling. To assess the role of IR in insulin-regulated glucose-stimulated insulin secretion (GSIS) compared with insulin-susceptible populations, US investigators studied 10 IGT patients, 11 T2DM patients and 8 healthy controls. Insulin secretion was assessed by infusion of normal saline or normal glucose-hyperinsulinemic clamp with B28-Asp-insulin for 4 h followed by dextrose administration for 80 min. The results showed that GSIS was increased in previously healthy subjects exposed to insulin. This effect is attenuated in people with IR, IGT and