Sensing of amino acids by the gut-expressed taste receptor T1R1-T1R3 stimulates CCK secretion
-
- Kristian Daly
- Epithelial Function and Development Group, Department of Functional and Comparative Genomics, University of Liverpool, Liverpool, United Kingdom;
-
- Miran Al-Rammahi
- Epithelial Function and Development Group, Department of Functional and Comparative Genomics, University of Liverpool, Liverpool, United Kingdom;
-
- Andrew Moran
- Epithelial Function and Development Group, Department of Functional and Comparative Genomics, University of Liverpool, Liverpool, United Kingdom;
-
- Marco Marcello
- Centre for Imaging, Institute of Integrative Biology, University of Liverpool, Liverpool, United Kingdom; and
-
- Yuzo Ninomiya
- Section of Oral Neuroscience, Graduate School of Dental Sciences, Kyushu University, Fukuoka, Japan
-
- Soraya P. Shirazi-Beechey
- Epithelial Function and Development Group, Department of Functional and Comparative Genomics, University of Liverpool, Liverpool, United Kingdom;
書誌事項
- 公開日
- 2013-02-01
- 資源種別
- journal article
- DOI
-
- 10.1152/ajpgi.00074.2012
- 公開者
- American Physiological Society
この論文をさがす
説明
<jats:p>CCK is secreted by endocrine cells of the proximal intestine in response to dietary components, including amino acids. CCK plays a variety of roles in digestive processes, including inhibition of food intake, consistent with a role in satiety. In the lingual epithelium, the sensing of a broad spectrum of l-amino acids is accomplished by the heteromeric amino acid (umami) taste receptor (T1R1-T1R3). T1R1 and T1R3 subunits are also expressed in the intestine. A defining characteristic of umami sensing by T1R1-T1R3 is its potentiation by IMP or GMP. Furthermore, T1R1-T1R3 is not activated by Trp. We show here that, in response to l-amino acids (Phe, Leu, Glu, and Trp), but not d-amino acids, STC-1 enteroendocrine cells and mouse proximal small intestinal tissue explants secrete CCK and that IMP enhances Phe-, Leu-, and Glu-induced, but not Trp-induced, CCK secretion. Furthermore, small interfering RNA inhibition of T1R1 expression in STC-1 cells results in significant diminution of Phe-, Leu-, and Glu-stimulated, but not Trp-stimulated, CCK release. In STC-1 cells and mouse intestine, gurmarin inhibits Phe-, Leu-, and Glu-induced, but not Trp-stimulated, CCK secretion. In contrast, the Ca<jats:sup>2+</jats:sup>-sensing receptor antagonist NPS2143 inhibits Phe-stimulated CCK release partially and Trp-induced CCK secretion totally in mouse intestine. However, NPS2143 has no effect on Leu- or Glu-induced CCK secretion. Collectively, our data demonstrate that functional characteristics and cellular location of the gut-expressed T1R1-T1R3 support its role as a luminal sensor for Phe-, Leu-, and Glu-induced CCK secretion.</jats:p>
収録刊行物
-
- American Journal of Physiology-Gastrointestinal and Liver Physiology
-
American Journal of Physiology-Gastrointestinal and Liver Physiology 304 (3), G271-G282, 2013-02-01
American Physiological Society