Bile deficiency induces changes in intestinal glucose absorption in mice
Bile deficiency induces changes in intestinal glucose absorption in mice
复制标题
胆汁缺乏会引起小鼠肠道葡萄糖吸收的变化。
DOI：
10.1016/j.surg.2016.05.040
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发表时间：
2016-12-01
期刊：
影响因子：
3.8
通讯作者：
Song, Penghong
中科院分区：
文献类型：
--
作者：
Du, Yehui;Chen, Hao;Song, Penghong
背景。胆道梗阻是一个常见的临床问题。在本研究中，我们试图了解胆道梗阻后肠道葡萄糖吸收的变化。
方法。建立小鼠胆管结扎和体外胆汁引流的实验模型。通过尤斯灌流室根据体外短路电流的增加以及体内口服葡萄糖后的血糖测量来检测小鼠肠道黏膜葡萄糖吸收情况。通过蛋白质印迹法和免疫组织化学法分析钠 - 葡萄糖协同转运蛋白1（SGLT1）和葡萄糖易化转运蛋白2（GLUT2）的蛋白表达。
结果。尤斯灌流室实验结果显示，在手术后1周和2周，胆管结扎和胆汁引流小鼠的十二指肠黏膜葡萄糖吸收水平显著高于正常对照小鼠。胃肠道给予胆汁酸几乎使胆汁引流小鼠升高的十二指肠黏膜葡萄糖吸收恢复到正常水平。体内实验结果进一步证实胆管结扎和胆汁引流小鼠的葡萄糖吸收增加。胆管结扎和胆汁引流小鼠十二指肠黏膜中SGLT1的蛋白表达水平均显著高于对照小鼠，而与对照小鼠相比，GLUT2的蛋白表达没有显著改变。
结论。肠道内胆汁缺乏会上调肠道黏膜SGLT1的表达，并增强肠道黏膜葡萄糖吸收能力，这有助于理解胆管梗阻和体外胆汁引流患者的肠道生理功能。（《外科学》2016年；160卷：1496 - 1507页）
Background. Biliary tract obstruction is a common clinical problem. In this study, we attempted to understand the change in intestinal glucose absorption after biliary tract obstruction.Methods. Experimental models of murine biliary duct ligation and external biliary drainage were established. Murine intestinal mucosal glucose absorption was examined with Ussing chambers according to the increase in the short-circuit current in vitro and blood glucose measurement after oral glucose in vivo. The protein expression of the sodium-glucose cotransporter (SGLT1) and the facilitated glucose transporter, member 2 (GLUT2) was analyzed by Western blot and immunohistochemistry.Results. The results from Ussing chamber experiments showed that duodenal mucosal glucose absorption levels were significantly higher in biliary duct ligation and biliary drainage mice than those in normal control mice at 1 and 2 weeks after the operation. Gastrointestinal bile acid administration almost reversed the elevated duodenal mucosal glucose absorption to the normal level in biliary drainage mice. The results from the experiments in vivo further confirmed that the glucose absorption increased in biliary duct ligation and biliary drainage mice. The protein expression levels of SGLT1 in the duodenal mucosae of both biliary duct ligation and biliary drainage mice were markedly higher than those in control mice, and the protein expression of GLUT2 was not significantly altered, compared with control mice.Conclusion. Bile deficiency in the intestine upregulates the expression of intestinal mucosal SGLT1 and enhances intestinal mucosal glucose absorption capacity, which contributes to the understanding of intestinal physiologic function for patients with biliary duct obstruction and external biliary drainage. (Surgery 2016; 160:1496-507.)