Intragastric administration of AMG517, a TRPV1 antagonist, enhanced activity-dependent energy metabolism via capsaicin-sensitive sensory nerves in mice. Issue 10 (2nd October 2020)

• Record Type: Journal Article
• Authors: Hai, Jun; Kawabata, Fuminori; Uchida, Kunitoshi; Nishimura, Shotaro; Tabata, Shoji
• Is Part Of: Bioscience, biotechnology, and biochemistry. Volume 84:Issue 10(2020)
• Page Start: 2121
• Page End: 2127
• Publication Date: 2020-10-02
• Subjects: AMG517 -- capsaicin-sensitive sensory nerves -- energy metabolism -- locomotor activity; Biotechnology -- Periodicals; Biochemistry -- Periodicals; 660.6
• DOI: 10.1080/09168451.2020.1789836
• Languages: English
• ISSNs: 0916-8451

Abstract

ABSTRACT: Transient receptor potential vanilloid 1 (TRPV1), a nociceptive cation channel, is known to play roles in regulating the energy metabolism (EM) of the whole body. We previously reported that TRPV1 antagonists such as AMG517 enhanced EM in mice, however, these mechanisms remain unclear. The aim of this study was to explore the mechanisms underlying the enhancement of EM by AMG517, a selective TRPV1 antagonist, in mice. Respiratory gas analysis indicated that intragastric administration of AMG517 enhanced EM along with increasing locomotor activity in mice. Next, to clarify the possible involvement with afferent sensory nerves, including the vagus, we desensitized the capsaicin-sensitive sensory nerves of mice by systemic capsaicin treatment. In the desensitized mice, intragastric administration of AMG517 did not change EM and locomotor activity. Therefore, this study indicated that intragastric administration of AMG517 enhanced EM and increased locomotor activity via capsaicin-sensitive sensory nerves, including vagal afferents in mice. Graphical Abstract: uf0001 Intragastric administration of AMG517, a TRPV1 antagonist, increases locomotor activity and enhances energy metabolism via capsaicin-sensitive sensory nerves in mice.