Effect of Atropine on Glucose-stimulated Gastric Inhibitory Polypeptide
Effect of Atropine on Glucose-stimulated Gastric Inhibitory Polypeptide
复制标题
阿托品对葡萄糖刺激胃抑制多肽的作用
DOI：
10.2337/diab.27.6.638
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发表时间：
1978
期刊：
影响因子：
7.7
通讯作者：
H. Mekhjian
中科院分区：
文献类型：
--
作者：
J. N. Larrimer;E. Mazzaferri;S. Cataland;H. Mekhjian
胃肠道胰岛素分泌的增加在很大程度上是由胃抑制多肽（GIP）介导的。由于增强胰岛素分泌的肠道信号被阿托品钝化，我们研究了这种药物对正常受试者葡萄糖刺激的GIP分泌的影响。对八名受试者进行了两次研究，给予十二指肠内葡萄糖（75克）。60分钟以上），静脉注射阿托品（15 μ g.每千克推注，随后为17 μ g。每分钟持续60分钟），另一次用静脉内盐水（对照）。比较阿托品和对照研究的结果，平均血清免疫反应性GIP（IRGIP）在5和15分钟时显著降低（444 ± 82 vs. 277 ± 44，p <0.05和1，072 ± 151 vs. 427 ± 74 pg./ ml.，5分钟和15分钟时p <0.02），阿托品组120分钟曲线下面积积分增量显著更小（62，170 ± 11，880 vs. 91，820 ± 14，200 pg. min. ml. -1 p <0.05）。在阿托品研究期间，血清IRI水平也显著较低（28 ± 8 vs. 14 ± 2，p <0.05，54 ± 7 vs. 25 ± 5，p <0.02，62 ± 8 vs. 36 ± 7 μ U）。每毫升，p <0.05，分别在15、30和45分钟）。阿托品使IRGIP曲线下面积的积分增量减少约33%，而IRI曲线下面积减少约45%。在第二组类似的实验中，用d-木糖代替葡萄糖，研究阿托品对正常受试者d-木糖吸收的影响。与对照研究相比，阿托品在第一个小时内没有改变d-木糖的吸收，但在第二个小时内显著增强了其吸收。我们的结论是，阿托品钝化了血清IRGIP的上升，通常刺激肠葡萄糖灌注，这可能是一个直接的影响，药物对胃肠道，而不是葡萄糖吸收的抑制介导的效果。这些观察结果与以下假设一致：GIP是增强胰岛素分泌的肠道信号，可被阿托品减弱。
Gastrointestinal augmentation of insulin secretion observed in response to glucose ingestion may be largely mediated by gastric inhibitory polypeptide (GIP). Since the enteric signal potentiating insulin secretion is blunted by atropine, we studied the effects of this drug on glucose-stimulated GIP secretion in normal subjects. Eight individuals, studied on two occasions, were given intraduodenal glucose (75 gm. over 60 minutes) by perfusion tube, on one occasion with intravenous atropine (15 μg. per kilogram bolus followed by 17 μg. per minute for 60 minutes) and on another occasion with intravenous saline (control). Comparing the results of atropine and control studies, mean serum immunoreactive GIP (IRGIP) was significantly lower at 5 and 15 minutes (444 ± 82 vs. 277 ± 44, p < 0.05 and 1,072 ± 151 vs. 427 ± 74 pg./ml., p < 0.02 at 5 and 15 minutes, respectively), and the integrated incremental area under the 120-minute curve was significantly less (62,170 ± 11,880 vs. 91,820 ± 14,200 pg. ·minute·ml.−1 p < 0.05) with atropine. Serum IRI levels were also significantly lower during the atropine studies (28 ± 8 vs. 14 ± 2, p < 0.05, 54 ± 7 vs. 25 ± 5, p < 0.02, 62 ± 8 vs. 36 ± 7 μU. per milliliter, p < 0.05, at 15, 30, and 45 minutes, respectively). The integrated incremental area under the IRGIP curve was reduced about 33 per cent, while the area under the IRI curve was reduced about 45 per cent by atropine. In a second group of similar experiments substituting d-xylose for glucose, the effect of atropine on d-xylose absorption was studied in normal subjects. Atropine did not alter d-xylose absorption during the first hour, but significantly enhanced its absorption during the second hour, as compared with control studies. We conclude that atropine blunts the rise in serum IRGIP normally stimulated by intestinal glucose perfusion, which is probably a direct effect of the drug on the gastrointestinal tract, as opposed to an effect mediated by inhibition of glucose absorption. These observations are consistent with the hypothesis that GIP is the enteric signal potentiating insulin secretion that is attenuated by atropine.