胰岛素对人体基础状态及胆囊收缩素刺激下胆囊运动的影响。

Effect of insulin on basal and cholecystokinin-stimulated gallbladder motility in humans.

作者信息

Gielkens H A, Lam W F, Coenraad M, Frölich M, van Oostayen J A, Lamers C B, Masclee A A

机构信息

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

出版信息

J Hepatol. 1998 Apr;28(4):595-602. doi: 10.1016/s0168-8278(98)80282-1.

DOI:10.1016/s0168-8278(98)80282-1

PMID:9566827

Abstract

BACKGROUND/AIMS: Acute hyperglycemia inhibits gallbladder contraction. In non-diabetic subjects this inhibitory effect may result from endogenous hyperinsulinemia. Therefore we investigated the effects of acute hyperglycemia and euglycemic hyperinsulinemia on basal and cholecystokinin-stimulated gallbladder motility.

METHODS

Gallbladder volume (ultrasonography) and duodenal bilirubin output were studied simultaneously in nine healthy volunteers (age 20-52 years) on 3 separate occasions in random order during: (a) saline infusion (control), (b) hyperglycemic hyperinsulinemic clamping (HG; plasma glucose at 15 mmol/l), and (c) euglycemic hyperinsulinemic clamping (HI; plasma insulin at 150 mU/l, glucose at 4-5 mmol/l). After a 2-h basal clamp period, cholecystokinin was infused intravenously for 60 min at 0.25 IDU x kg(-1) x h(-1), followed by another 60 min at 0.5 IDU x kg(-1) x h(-1).

RESULTS

HI and HG significantly (p<0.05) reduced basal duodenal bilirubin output compared to control, while basal gallbladder volume did not change. At the low dose cholecystokinin, gallbladder emptying during HG (25+/-3%) and HI (39+/-4%) was significantly (p<0.01) reduced compared to control (61+/-4%). The inhibitory effect of HG was significantly (p<0.05) stronger compared to HI. Duodenal bilirubin output during the low dose cholecystokinin was significantly (p<0.05) reduced by HG, but not by HI. No inhibitory effect of HG and HI on gallbladder emptying and duodenal bilirubin output was observed with the high dose of cholecystokinin.

CONCLUSIONS

In healthy subjects acute hyperglycemia and euglycemic hyperinsulinemia reduce basal duodenal bilirubin output and inhibit gallbladder emptying stimulated by low dose cholecystokinin. These results suggest that insulin is involved in the inhibitory effect of hyperglycemia on basal and cholecystokinin-stimulated gallbladder motility.

摘要

背景/目的：急性高血糖会抑制胆囊收缩。在非糖尿病患者中，这种抑制作用可能源于内源性高胰岛素血症。因此，我们研究了急性高血糖和正常血糖高胰岛素血症对基础状态及胆囊收缩素刺激的胆囊运动的影响。

方法

在9名健康志愿者（年龄20 - 52岁）中，通过超声检查同时研究胆囊体积，并在3个不同时间随机进行以下操作，以测量十二指肠胆红素输出量：（a）输注生理盐水（对照），（b）高血糖高胰岛素钳夹（HG；血浆葡萄糖浓度为15 mmol/l），以及（c）正常血糖高胰岛素钳夹（HI；血浆胰岛素浓度为150 mU/l，葡萄糖浓度为4 - 5 mmol/l）。在2小时的基础钳夹期后，以0.25 IDU×kg⁻¹×h⁻¹的速率静脉输注胆囊收缩素60分钟，随后以0.5 IDU×kg⁻¹×h⁻¹的速率再输注60分钟。

结果

与对照相比，HI和HG显著（p<0.05）降低了基础十二指肠胆红素输出量，而基础胆囊体积未发生变化。在低剂量胆囊收缩素作用下，HG（25±3%）和HI（39±4%）时的胆囊排空与对照（61±4%）相比显著（p<0.01）降低。与HI相比，HG的抑制作用显著更强（p<0.05）。低剂量胆囊收缩素作用期间，HG显著（p<0.05）降低了十二指肠胆红素输出量，但HI未使其降低。高剂量胆囊收缩素作用下，未观察到HG和HI对胆囊排空及十二指肠胆红素输出有抑制作用。