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大鼠空肠内功能性活跃的甜味受体缺失。

Lack of functionally active sweet taste receptors in the jejunum in vivo in the rat.

机构信息

Department of Surgery and Gastroenterology Research Unit, Mayo Clinic, Rochester, MN 55905, USA.

出版信息

J Surg Res. 2013 Aug;183(2):606-11. doi: 10.1016/j.jss.2013.02.031. Epub 2013 Mar 13.

Abstract

BACKGROUND

When studied in enterocyte-like cell lines (Caco-2 and RIE cells), agonists and antagonists of the sweet taste receptor (STR) augment and decrease glucose uptake, respectively. We hypothesize that exposure to STR agonists and antagonists in vivo will augment glucose absorption in the rat.

MATERIALS AND METHODS

About 30-cm segments of jejunum in anesthetized rats were perfused with iso-osmolar solutions containing 10, 35, and 100 mM glucose solutions (n = 6 rats, each group) with and without the STR agonist 2 mM acesulfame potassium and the STR inhibitor 10 μM U-73122 (inhibitor of the phospholipase C pathway). Carrier-mediated absorption of glucose was calculated by using stereospecific and nonstereospecific (14)C-d-glucose and (3)H-l-glucose, respectively.

RESULTS

Addition of the STR agonist acesulfame potassium to the 10, 35, and 100 mM glucose solutions had no substantive effects on glucose absorption from 2.1 ± 0.2 to 2.0 ± 0.3, 5.8 ± 0.2 to 4.8 ± 0.2, and 15.5 ± 2.3 to 15.7 ± 2.7 μmoL/min/30-cm intestinal segment (P > 0.05), respectively. Addition of the STR inhibitor (U-73122) also had no effect on absorption in the 10, 35, and 100 mM solutions from 2.3 ± 0.1 to 2.1 ± 0.2, 7.7 ± 0.5 to 7.2 ± 0.5, and 15.7 ± 0.9 to 15.2 ± 1.1 μmoL/min/30-cm intestinal segment, respectively.

CONCLUSIONS

Provision of glucose directly into rat jejunum does not augment glucose absorption via STR-mediated mechanisms within the jejunum in the rat. Our experiments show either no major role of STRs in mediating postprandial augmentation of glucose absorption or that proximal gastrointestinal tract stimulation of STR or other luminal factors may be required for absorption of glucose to be augmented by STR.

摘要

背景

当在肠上皮样细胞系(Caco-2 和 RIE 细胞)中进行研究时,甜味受体(STR)的激动剂和拮抗剂分别增加和减少葡萄糖摄取。我们假设在体内暴露于 STR 激动剂和拮抗剂会增加大鼠的葡萄糖吸收。

材料和方法

在麻醉大鼠的约 30cm 空肠段中,用等渗溶液灌注 10、35 和 100mM 葡萄糖溶液(n = 6 只大鼠,每组),同时加入 STR 激动剂 2mM 乙酰磺胺酸钾和 STR 抑制剂 10μM U-73122(磷脂酶 C 途径抑制剂)。通过使用立体特异性和非立体特异性(14)C-d-葡萄糖和(3)H-l-葡萄糖分别计算葡萄糖的载体介导吸收。

结果

将 STR 激动剂乙酰磺胺酸钾加入到 10、35 和 100mM 葡萄糖溶液中,对 2.1±0.2 至 2.0±0.3、5.8±0.2 至 4.8±0.2 和 15.5±2.3 至 15.7±2.7μmoL/min/30-cm 肠段的葡萄糖吸收没有实质性影响(P>0.05)。添加 STR 抑制剂(U-73122)也没有影响 10、35 和 100mM 溶液中的吸收,从 2.3±0.1 至 2.1±0.2、7.7±0.5 至 7.2±0.5 和 15.7±0.9 至 15.2±1.1μmoL/min/30-cm 肠段,分别。

结论

直接向大鼠空肠提供葡萄糖不会通过 STR 介导的机制增加大鼠空肠中的葡萄糖吸收。我们的实验表明,STR 在介导餐后葡萄糖吸收增加中没有主要作用,或者近端胃肠道刺激 STR 或其他腔内容物可能是通过 STR 增加葡萄糖吸收所必需的。

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本文引用的文献

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J Gastrointest Surg. 2013 Jan;17(1):153-8; discussion p. 158. doi: 10.1007/s11605-012-1998-z. Epub 2012 Sep 5.
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