Studies of secretin-stimulated insulin responses in man.

Studies of secretin-stimulated insulin responses in man.
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促胰液素刺激的人类胰岛素反应的研究。

DOI:
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发表时间:
1972
影响因子:
15.9
通讯作者:
D. Porte
D. Porte
中科院分区:
医学1区
文献类型:
--
作者:
R. Lerner;D. Porte

文献摘要

被引文献

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最近的研究表明,胰泌素,像葡萄糖,刺激一个快速的胰岛素反应从一个小的存储池。为了评价促胰液素刺激的胰岛素反应的机制,在20小时300 mg/min葡萄糖输注之前、期间和之后给予小剂量(15 U)快速静脉注射(脉冲)促胰液素。与先前的研究相反,表明与对预输注脉冲的响应相比,对葡萄糖输注开始后45分钟给予的小(5 g)葡萄糖脉冲的急性胰岛素响应显著减弱,(2-5分钟δ免疫反应性胰岛素μ U/ml)对15-U促胰液素脉冲的刺激显示出大于两倍的增加,(治疗前:31.1 ± 15.4;治疗中:71.2 ± 40.4,muU/ml,平均值± SD,P < 0.02)。在连续葡萄糖输注20小时后也发现对胰泌素的反应增加,但在停止输注1小时后,当血糖水平恢复至对照值时,未观察到对胰泌素的反应增加。因此,这种对促胰液素的增加的反应是葡萄糖依赖性的。以30分钟间隔给予4次150-U促胰液素脉冲,每次后续脉冲均引起急性胰岛素反应逐渐显著降低,与小储存池耗尽一致。类似于观察到的胰岛素对促胰液素的响应幅度是葡萄糖依赖性的,葡萄糖刺激的输出似乎是促胰液素依赖性的。因此,促胰液素预处理后,对5 g葡萄糖的急性胰岛素反应增加(促胰液素前:34.9 ± 14.8;促胰液素后:50.5 ± 22.5 μ U/ml。P < 0.02),提示促胰液素可扩大葡萄糖刺激的贮血池或增加其敏感性。肾上腺素和普萘洛尔对促胰液素和葡萄糖的急性胰岛素反应的影响也不同。15-U促胰液素脉冲不受肾上腺素(前:31.6+/-17.9;期间:27.8+/-16.6 muU/ml)或普萘洛尔(前:12.8+/-8.4;期间:10.7+/-5.5 muU/ml)输注的影响。这些研究的结果表明,虽然葡萄糖和胰泌素都能刺激快速的胰岛素反应,但这些反应很容易区分。这些数据表明,葡萄糖和胰泌素刺激功能上独立的胰岛素储存池,但对任何刺激的急性反应部分取决于对另一种刺激的暴露。
Recent studies have suggested that secretin, like glucose, stimulates a rapid insulin response from a small storage pool. In order to evaluate the mechanism of the secretin-stimulated insulin response, small (15 U) rapidly administered intravenous injections (pulses) of secretin were given before, during, and after a 20 hr 300 mg/min glucose infusion. Contrary to previous studies demonstrating that the acute insulin response to a small (5 g) pulse of glucose given 45 min after the start of the glucose infusion was significantly diminished compared to the response to the preinfusion pulse, the acute insulin response (2-5 min Deltaimmuno-reactive insulin muU/ml) to 15-U secretin pulses exhibited a greater than twofold increase (before: 31.1+/-15.4; during: 71.2+/-40.4, muU/ml, mean +/-SD, P < 0.02). The increased response to secretin was also found after 20 hr of continuous glucose infusion, but was not observed 1 hr after cessation of the infusion when plasma glucose levels returned to control values. Thus, this increased response to secretin was glucose dependent. Four 150-U secretin pulses given at 30 min intervals elicited progressively and significantly diminished acute insulin responses with each succeeding pulse, consistent with depletion of the small storage pool. Similar to the observation that the magnitude of the insulin response to secretin was glucose dependent, the glucose-stimulated output appeared to be secretin dependent. Thus the acute insulin response to 5 g glucose was increased after secretin pretreatment (presecretin: 34.9+/-14.8; postsecretin: 50.5+/-22.5 muU/ml. P < 0.02) which suggests that secretin may either enlarge the storage pool stimulated by glucose or increase its sensitivity. The effect of epinephrine and propranolol on acute insulin responses to secretin and glucose was also different. 15-U secretin pulses were unaffected by infusions of either epinephrine (pre: 31.6+/-17.9; during: 27.8+/-16.6 muU/ml) or propranolol (pre: 12.8+/-8.4; during: 10.7+/-5.5 muU/ml). The results of these studies indicate that although both glucose and secretin stimulate a rapid insulin response, these responses are easily differentiated. The data suggest that glucose and secretin stimulate functionally separate storage pools of insulin, but that the acute response to either stimulus is partly determined by exposure to the other.