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健康与糖尿病状态下碳水化合物消化及胰多肽的释放

Carbohydrate digestion and release of pancreatic polypeptide in health and diabetes mellitus.

作者信息

Layer P, Go V L, DiMagno E P

机构信息

Division of Gastroenterology, Mayo Clinic, Rochester, MN.

出版信息

Gut. 1989 Sep;30(9):1279-84. doi: 10.1136/gut.30.9.1279.

DOI:10.1136/gut.30.9.1279
PMID:2478426
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1434239/
Abstract

The effects of meal volume and luminal digestion of carbohydrates on the release of pancreatic polypeptide (HPP) were investigated in eight healthy subjects and in six patients who had non-insulin dependent diabetes mellitus. On one occasion each subject ingested a placebo with 200 ml water and a starch (50 g) pudding meal (400 ml) 30 minutes later. On another occasion an amylase inhibitor that retards intraluminal starch digestion was given with the water and starch. In normal subjects, water caused a moderate rise in HPP plasma levels (16.9 (10.9) pg/ml; p less than 0.02) and ingestion of starch increased HPP in a double peaked pattern. The mean increments of the peaks were 45.0 (15.2) pg/ml (p less than 0.02) and 41.1 (17.3) pg/ml (p less than 0.05), respectively. In the diabetic subjects, the HPP concentrations did not increase in response to water. After ingestion of starch the diabetics had two peaks of HPP that were similar in magnitude, but the early postprandial peak was delayed significantly compared to normal subjects (37.5 (5.1) min v 23.4 (3.9) min; p less than 0.05). The amylase inhibitor (5 or 10 g) reduced the early postprandial HPP peak by 79% (p less than 0.05) in normal subjects and 4 g of the inhibitor reduced the early HPP peak by 58% (p less than 0.05) in the diabetics. In both groups ingestion of the amylase inhibitor abolished the late HPP peak (p less than 0.05). In conclusion, carbohydrate induced HPP release is dependent on undisturbed intraluminal starch digestion.

摘要

在8名健康受试者和6名非胰岛素依赖型糖尿病患者中,研究了进餐量和碳水化合物腔内消化对胰多肽(HPP)释放的影响。每位受试者在一个时间段摄入含200毫升水的安慰剂,30分钟后摄入一份淀粉(50克)布丁餐(400毫升)。在另一个时间段,将一种延缓腔内淀粉消化的淀粉酶抑制剂与水和淀粉一起给予。在正常受试者中,水导致HPP血浆水平适度升高(16.9(10.9)皮克/毫升;p<0.02),摄入淀粉使HPP呈双峰模式增加。峰值的平均增量分别为45.0(15.2)皮克/毫升(p<0.02)和41.1(17.3)皮克/毫升(p<0.05)。在糖尿病受试者中,HPP浓度对水无反应性增加。摄入淀粉后,糖尿病患者有两个幅度相似的HPP峰值,但餐后早期峰值与正常受试者相比明显延迟(37.5(5.1)分钟对23.4(3.9)分钟;p<0.05)。淀粉酶抑制剂(5或10克)使正常受试者餐后早期HPP峰值降低79%(p<0.05),4克该抑制剂使糖尿病患者早期HPP峰值降低58%(p<0.05)。在两组中,摄入淀粉酶抑制剂均消除了HPP晚期峰值(p<0.05)。总之,碳水化合物诱导的HPP释放依赖于未受干扰的腔内淀粉消化。

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引用本文的文献

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Pancreas. 2014 May;43(4):651-6. doi: 10.1097/MPA.0000000000000082.

本文引用的文献

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Release of pancreatic polypeptide in humans by infusion of cholecystokinin.通过输注胆囊收缩素在人体中释放胰多肽。
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Gastric motor abnormalities in diabetic and postvagotomy gastroparesis: effect of metoclopramide and bethanechol.糖尿病性胃轻瘫和迷走神经切断术后胃轻瘫的胃运动异常:胃复安和氨甲酰甲胆碱的作用
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Dose-dependent increase in concentrations of gastric inhibitory polypeptide and pancreatic polypeptide after small amounts of glucose intraduodenally in man.人体十二指肠内注入少量葡萄糖后,胃抑制性多肽和胰多肽浓度呈剂量依赖性增加。
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Impaired pancreatic polypeptide responses to insulin-induced hypoglycemia in diabetic autonomic neuropathy.糖尿病自主神经病变中胰腺多肽对胰岛素诱导的低血糖反应受损。
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Identification of type I diabetic patients at increased risk for hypoglycemia during intensive therapy.识别强化治疗期间低血糖风险增加的1型糖尿病患者。
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