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急性高血糖对人体基础和蛙皮素刺激的胰胆分泌的影响。

Effect of acute hyperglycemia on basal and bombesin-stimulated pancreaticobiliary secretion in humans.

作者信息

Lam W F, Masclee A A, Muller E S, Souverijn J H, Lamers C B

机构信息

Department of Gastroenterology-Hepatology, Leiden University Medical Center, The Netherlands.

出版信息

Pancreas. 1998 Aug;17(2):201-7. doi: 10.1097/00006676-199808000-00015.

DOI:10.1097/00006676-199808000-00015
PMID:9700954
Abstract

This study was undertaken to investigate the effect of acute hyperglycemia on basal and bombesin-stimulated pancreaticobiliary secretion. Seven healthy subjects participated in two experiments performed in random order during normoglycemia and hyperglycemic clamping at 15 mM. Duodenal outputs of bilirubin, trypsin, amylase, and bicarbonate were measured by aspiration with a recovery marker under basal conditions for 60 min and during continuous infusion of bombesin (1 ng/kg x min) for 60 min. Plasma cholecystokinin (CCK) and pancreatic polypeptide (PP) levels were determined at regular intervals. Compared to normoglycemia, during hyperglycemia basal outputs of bilirubin (17 +/- 3 vs. 0.9 +/- 0.4 micromol/60 min), trypsin (24 +/- 4 vs. 4 +/- 1 U/60 min), amylase (12 +/- 1 vs. 3 +/- 1 kU/60 min), and bicarbonate (2.9 +/- 0.5 vs. 1.2 +/- 0.2 mmol/60 min) were significantly p < 0.05) reduced. Bombesin significantly (p < 0.05) increased pancreaticobiliary output during both normo- and hyperglycemia. During hyperglycemia bombesin-stimulated 60-min outputs of bilirubin, trypsin, amylase, and bicarbonate were not significantly different compared to those during normoglycemia. Basal and bombesin-stimulated plasma PP concentrations were significantly (p < 0.05) reduced during hyperglycemia, but plasma CCK levels were not significantly different. It is concluded that acute hyperglycemia reduces basal but does not affect bombesin-induced pancreaticobiliary secretion.

摘要

本研究旨在探讨急性高血糖对基础状态下及蛙皮素刺激的胰胆分泌的影响。七名健康受试者参与了两项实验,实验在正常血糖和血糖钳制在15 mM的高血糖状态下随机进行。在基础状态下60分钟以及持续输注蛙皮素(1 ng/kg·min)60分钟期间,通过使用回收标记物抽吸来测量十二指肠中胆红素、胰蛋白酶、淀粉酶和碳酸氢盐的输出量。定期测定血浆胆囊收缩素(CCK)和胰多肽(PP)水平。与正常血糖相比,高血糖期间胆红素的基础输出量(17±3 vs. 0.9±0.4 μmol/60分钟)、胰蛋白酶(24±4 vs. 4±1 U/60分钟)、淀粉酶(12±1 vs. 3±1 kU/60分钟)和碳酸氢盐(2.9±0.5 vs. 1.2±0.2 mmol/60分钟)均显著降低(p<0.05)。在正常血糖和高血糖状态下,蛙皮素均显著(p<0.05)增加胰胆分泌量。在高血糖期间,蛙皮素刺激60分钟的胆红素、胰蛋白酶、淀粉酶和碳酸氢盐输出量与正常血糖期间相比无显著差异。高血糖期间基础状态下和蛙皮素刺激后的血浆PP浓度显著降低(p<0.05),但血浆CCK水平无显著差异。结论。结论是急性高血糖会降低基础胰胆分泌,但不影响蛙皮素诱导的胰胆分泌。

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