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TRPA1 激动剂，甲基丁香酚可抑制食物摄入和胃排空。

The TRPA1 agonist, methyl syringate suppresses food intake and gastric emptying.

机构信息

Division of Metabolism and Functionality Research, Korea Food Research Institute, Bundang-gu, Sungnam-si, Gyeonggi-do, South Korea.

出版信息

PLoS One. 2013 Aug 21;8(8):e71603. doi: 10.1371/journal.pone.0071603. eCollection 2013.

DOI:10.1371/journal.pone.0071603
PMID:23990963
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3749221/
Abstract

Transient receptor potential channel ankryn 1 (TRPA1) expressed in the gastrointestinal tract is associated with gastric motility, gastric emptying, and food intake. In this study, we investigated the effects of methyl syringate, a specific and selective TRPA1 agonist, on food intake, gastric emptying, and gut hormone levels in imprinting control region (ICR) mice. The administration of methyl syringate suppressed cumulative food intake and gastric emptying. In addition, treatment with ruthenium red (RR), a general cation channel blocker, and HC-030031, a selective TRPA1 antagonist, inhibited methyl syringate-induced reduction of food intake and delayed gastric emptying in ICR mice. Methyl syringate also increased plasma peptide YY (PYY) levels, but not glucagon-like peptide-1 (GLP-1) levels. The elevation in PYY was blocked by treatment with RR and HC-030031. The present findings indicate that methyl syringate regulates food intake and gastric emptying through a TRPA1-mediated pathway and, by extension, can contribute to weight suppression.

摘要

瞬时受体电位通道锚蛋白 1（TRPA1）在胃肠道中表达，与胃动力、胃排空和摄食有关。在这项研究中，我们研究了甲基丁香酚，一种特异性和选择性的 TRPA1 激动剂，对印迹控制区（ICR）小鼠摄食、胃排空和肠道激素水平的影响。甲基丁香酚的给药抑制了累积的食物摄入和胃排空。此外，用通用阳离子通道阻滞剂钌红（RR）和选择性 TRPA1 拮抗剂 HC-030031 处理，抑制了甲基丁香酚诱导的 ICR 小鼠摄食减少和胃排空延迟。甲基丁香酚还增加了血浆肽 YY（PYY）水平，但不增加胰高血糖素样肽-1（GLP-1）水平。RR 和 HC-030031 的处理阻断了 PYY 的升高。这些发现表明，甲基丁香酚通过 TRPA1 介导的途径调节摄食和胃排空，并可促进体重抑制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5a2/3749221/72c66415e78e/pone.0071603.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5a2/3749221/a13fbcf4d97d/pone.0071603.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5a2/3749221/cd23ad411494/pone.0071603.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5a2/3749221/27c6f8200a93/pone.0071603.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5a2/3749221/de62fcc1522f/pone.0071603.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5a2/3749221/0d7ad5465f0c/pone.0071603.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5a2/3749221/72c66415e78e/pone.0071603.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5a2/3749221/a13fbcf4d97d/pone.0071603.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5a2/3749221/cd23ad411494/pone.0071603.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5a2/3749221/27c6f8200a93/pone.0071603.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5a2/3749221/de62fcc1522f/pone.0071603.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5a2/3749221/0d7ad5465f0c/pone.0071603.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5a2/3749221/72c66415e78e/pone.0071603.g006.jpg

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