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, 8 (8), e71603
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The TRPA1 Agonist, Methyl Syringate Suppresses Food Intake and Gastric Emptying

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The TRPA1 Agonist, Methyl Syringate Suppresses Food Intake and Gastric Emptying

Min Jung Kim et al. PLoS One.

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.

Conflict of interest statement

Competing Interests: The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1. Chemical structures of cinnamaldehyde and methyl syringate.
Figure 2
Figure 2. Effects of cinnamaldehyde (CALD) and methyl syringate (MS) on cumulative food intake.
Vehicle (1.5% methyl cellulose), CALD, or MS were administered orally to ICR mice at a dose of 10 mg/kg after fasting in the presence or absence of the TRPA1 antagonists RR and HC-030031. Mice were allowed free access to normal food and water immediately after treatment. Changes in cumulative food intake were monitored for 28 h. Data represent means ± SEM (n = 4); *p<0.05 compared with the vehicle group by Dunnett's test.
Figure 3
Figure 3. Effect of cinnamaldehyde (CALD) and methyl syringate (MS) on food remaining in the stomach.
Vehicle (1.5% methyl cellulose), CALD, or MS were administered orally to ICR mice at a dose of 10 mg/kg after fasting in the presence or absence of the TRPA1 antagonists, ruthenium red (RR) and HC-030031. After 28 h, mice were sacrificed and the stomach contents of each were weighed. Columns and vertical bars represent means ± SEM (n = 4); *p<0.05 compared with the vehicle control.
Figure 4
Figure 4. Effects of cinnamaldehyde (CALD) and methyl syringate (MS) on gastric emptying.
Phenol red was administered 5 min after treatment with vehicle (1.5% methyl cellulose), CALD (0.1–80 mg/kg) and MS (0.1–10 mg/kg). Gastric emptying was evaluated by measuring the quantity of phenol red retained in the stomach 15 min after administration. Columns and vertical bars represent means ± SEM (n = 4); *p<0.05 compared with the vehicle control.
Figure 5
Figure 5. Inhibitory effect of ruthenium red (RR) or HC-030031 on gastric emptying in mice treated with cinnamaldehyde (CALD) or methyl syringate (MS).
Phenol red was administered 5 min after treatment with vehicle (1.5% methyl cellulose), CALD, or MS at a dose of 10 mg/kg in the presence or absence of RR (A) and HC-030031 (B). Gastric emptying was evaluated measuring the quantity of phenol red retained in the stomach after 15 min. Columns and vertical bars represent the means ± SEM (n = 4); *p<0.05 compared with the vehicle control.
Figure 6
Figure 6. Effects of cinnamaldehyde (CALD) or methyl syringate (MS) on plasma PYY and glucagon-like peptide (GLP-1) levels.
Vehicle (1.5% methyl cellulose), CALD, or MS were administered orally to ICR mice at a dose of 10 mg/kg after fasting in the presence or absence of the TRPA1 antagonists RR and HC-030031. Plasma PYY (A) or GLP-1 levels (B) upon CALD and MS treatment alone or with the addition of RR and HC-030031 (C) were evaluated at 0 min and 15 min and relative values calculated. Columns and vertical bars represent means ± SEM (n = 4); *p<0.05 compared with the vehicle control.

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Grant support

This study was supported by Korea Food Research Institute (E0131201). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
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