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J Vet Sci 2018; 19(2): 179-187  https://doi.org/10.4142/jvs.2018.19.2.179
Calcium-sensing receptor-mediated L-tryptophan-induced secretion of cholecystokinin and glucose-dependent insulinotropic peptide in swine duodenum
Xiuying Zhao, Yihan Xian, Chao Wang, Liren Ding, Xianglong Meng, Weiyun Zhu, Suqin Hang*
Laboratory of Gastrointestinal Microbiology, Nanjing Agricultural University, Nanjing 210095, China
Correspondence to: Tel: +86-25-84395037; Fax: +86-25-84395314; E-mail: suqinhang69@njau.edu.cn
The first two authors contributed equally to this work.
Received: August 7, 2017; Revised: December 17, 2017; Accepted: December 26, 2017; Published online: March 31, 2018.
This study aimed to elucidate the effect of tryptophan (Trp) on gut hormone secretion as well as the roles of the calcium-sensing receptor (CaSR) and its downstream signaling pathway in gut hormone secretion by assessing swine duodenal perfusion in vitro. Swine duodenum was perfused with Krebs-Henseleit buffer as a basal solution. Various concentrations (0, 10, and 20 mM) of Trp were applied to investigate its effect on gut hormone secretion. A CaSR antagonist was used to detect the involvement of CaSR and its signal molecules. The 20 mM Trp concentration promoted the secretion of cholecystokinin (CCK) and glucose-dependent insulinotropic peptide (GIP), elevated the mRNA level of CaSR, and upregulated the protein levels of CaSR, protein kinase C (PKC), and inositol trisphosphate receptor (IP3R). However, NPS 2143, an inhibitor of CaSR, attenuated the CCK and GIP release, reduced the mRNA level of CaSR, and decreased the protein levels of CaSR, PKC, and IP3R with 20 mM Trp perfusion. The results indicate that CCK and GIP secretion can be induced by Trp in swine duodenum in vitro, and the effect is mediated by CaSR and its downstream signal molecules PKC and IP3R.
Keywords: calcium-sensing receptor, gut hormone, signaling pathway, swine, tryptophan

© 2018 The Korean Society of Veterinary Science.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.