Eur J Pharmacol
Institute of Biochemistry and Molecular Biology, School of Life Sciences, Key Laboratory of Preclinical Study for New Drugs of Gansu Province, Lanzhou University, Lanzhou 730000, China. Electronic address:
Published: January 2017
Kisspeptin (KP), the endogenous ligand of GPR54, is a mammalian amidated neurohormone, which belongs to the RF-amide peptide family. However, in contrast with the related members of the RF-amide family, little information is available regarding its role in the gastrointestinal motility. With regard to the recent data suggesting KP play an important role in food intake, and while gastrointestinal motility are closely related to it. Thus, in the present work, effects of central administration of KP-13, one of the endogenous active isoforms, on gastrointestinal motility were investigated. The results indicated that intracerebroventricular (i.c.v.) infused of KP-13 significantly facilitated gastrointestinal transit, bead expulsion and fecal pellet output, respectively, while has no effect on gastric emptying. The effects were significantly reversed by GPR54 antagonist 234, but not GnRH receptor antagonist Cetrorelix. However, i.p. injected of KP-13 or compound 5 (10mg/kg), a high metabolic stability kisspeptin analog, did not affect gastrointestinal transit, suggesting that KP-13 or compound 5 facilitated gastrointestinal transit through the activation of central GPR54. Then the gastrointestinal motility-enhancing effects were also presented after infusion of KP-13 into the hypothalamus. In vitro, KP-13 (10M) also modulated colonic contraction, but not in the stomach and small intestine. Similarly, KP-13 (10M)-induced contractions of circular and longitudinal colonic muscle were significantly attenuated by antagonist 234 (10M). In conclusion, all the results indicated that KP-13 promoted gastrointestinal motility through the activation of GPR54, which implicate that KP/GPR54 system might be a new target to treat gastrointestinal function disorder.
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http://dx.doi.org/10.1016/j.ejphar.2016.11.041 | DOI Listing |
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