L‐Ornithine and l‐lysine stimulate gastrointestinal motility via transient receptor potential vanilloid 1. Issue 11 (7th September 2017)

• Record Type: Journal Article
• Authors: Nakato, Junya; Ho, Yee Yin; Omae, Ryo; Mizushige, Takafumi; Uchida, Kunitoshi; Tominaga, Makoto; Kim, Minji; Goto, Tsuyoshi; Takahashi, Nobuyuki; Kawada, Teruo; Akiduki, Saori; Kanamoto, Ryuhei; Ohinata, Kousaku
• Is Part Of: Molecular nutrition & food research. Volume 61:Issue 11(2017)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2017-09-07
• Subjects: Basic amino acids -- Gastrointestinal motility -- Muscarinic acetylcholine receptor -- Nitric oxide synthase -- Transient receptor potential vanilloid 1; Food -- Biotechnology -- Periodicals; Food -- Microbiology -- Periodicals; Nutrition -- Periodicals; Food -- Toxicology -- Periodicals; Nutrition -- Periodicals; Food Microbiology -- Periodicals; Food Technology -- Periodicals; Molecular Biology -- Periodicals; 664.0705
• DOI: 10.1002/mnfr.201700230
• Languages: English
• ISSNs: 1613-4125

Abstract

Abstract : Scope: The gastrointestinal (GI) tract senses and responds to intraluminal nutrients and these interactions often affect GI functions. We found that, among basic amino acids, l ‐ornithine (Orn) andl ‐lysine (Lys) stimulated butl ‐arginine (Arg) suppressed GI motility after oral administration (24 mmol/kg) in mice (Orn and Lys, 14.3 and 26.4% promotion; Arg, 7.7% suppression). We investigated the mechanism of the action of Orn and Lys on GI motility. Methods and results: Orn‐induced promotion of small intestinal transit was significantly inhibited ( p <0.05) by oral administration of capsazepine, a transient receptor potential vanilloid 1 (TRPV1) antagonist. Moreover, the stimulatory effect of Orn and Lys was abolished in TRPV1‐knockout mice. In TRPV1‐transfected HEK293 cells, Orn and Lys (10 mM) evoked Ca 2+ influx, which was blocked by ruthenium red, a TRP channel antagonist. These results suggest that Orn and Lys promote GI motility via activation of TRPV1. The GI motility stimulation by Orn and Lys was also blocked by atropine, a muscarinic acetylcholine receptor (mAChR) antagonist, or N G ‐nitro‐l ‐arginine methyl ester, a nitric oxide (NO) synthase inhibitor. Conclusion: Orally administered Orn and Lys stimulate GI motility via TRPV1, mAChR and NO synthase in mice. Abstract : Among basic amino acids, l ‐ornithine (Orn) andl ‐lysine (Lys) stimulated butl ‐arginine (Arg) suppressed gastrointestinal (GI) motility after oral administration. Orn‐ and Lys‐induced GI motility stimulation was inhibited by either TRPV1 antagonist or TRPV1‐knockout mice. The stimulatory effect of Orn and Lys on GI motility was also mediated by muscarinic acetylcholine receptor and nitric oxide synthase.