Phenylalanine and tryptophan stimulate gastrin and somatostatin secretion and H+-K+-ATPase activity in pigs through calcium-sensing receptor
•Phe and Trp stimulate hormone secretion and H+-K+-ATPase activity in pigs.•CaSR mediates hormone secretion and H+-K+-ATPase activity induced by Phe and Trp.•The downstream signaling molecular IP3R is involved in the mediation of CaSR. In rodents and humans, aromatic amino acids increase gut hormone...
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Published in | General and comparative endocrinology Vol. 267; pp. 1 - 8 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
01.10.2018
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Subjects | |
Online Access | Get full text |
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Summary: | •Phe and Trp stimulate hormone secretion and H+-K+-ATPase activity in pigs.•CaSR mediates hormone secretion and H+-K+-ATPase activity induced by Phe and Trp.•The downstream signaling molecular IP3R is involved in the mediation of CaSR.
In rodents and humans, aromatic amino acids increase gut hormone secretion and H+-K+-ATPase activity by modulating calcium-sensing receptor (CaSR). However, the role of CaSR and its related signaling molecules in amino acid-induced gut hormone secretion in swine has not been investigated. Here, we examined whether a CaSR-dependent pathway modulated gastrin and somatostatin (SS) secretion and H+-K+-ATPase activity in pigs. Perfusion of pig stomach tissues in the presence of extracellular 80 mM l-phenylalanine (Phe) or 20 mM l-tryptophan (Trp) and a CaSR agonist cinacalcet triggered gastrin and SS secretion and H+-K+-ATPase activity (P < 0.05) and increased CaSR expression (P < 0.05). This effect of Phe and Trp was dependent on Ca2+ (P < 0.05) and was abolished after treatment with NPS 2143, an inhibitor of CaSR, and 2-aminoethyl diphenyl borinate, an inhibitor of CaSR downstream signaling molecule inositol 1,4,5-triphosphate receptor (IP3R). These findings indicate that Phe and Trp induce Ca2+-dependent gastrin and SS secretion and H+-K+-ATPase activity through CaSR and its downstream signaling molecule IP3R. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0016-6480 1095-6840 |
DOI: | 10.1016/j.ygcen.2018.05.022 |