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Bitter receptors and glucose transporters interact to control carbohydrate and immune responses in the gut
Author(s) -
Palatini Kimberly M,
Durand PierJean,
Rathinasabapathy Thirumurugan,
Esposito Debora,
Komarnytsky Slavko
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.682.6
Subject(s) - glucose transporter , gpr120 , enteroendocrine cell , glut2 , carbohydrate metabolism , biology , glucose uptake , postprandial , taste receptor , incretin , receptor , biochemistry , pharmacology , endocrinology , diabetes mellitus , insulin , g protein coupled receptor , type 2 diabetes , hormone , endocrine system
Receptors of bitter taste (T2Rs) co‐localize with glucose transporters SGLT‐1, GLUT2 and GLUT5 in the gastrointestinal enterocytes and enteroendocrine cells. Since plant‐based foods are the primary source of both carbohydrates and bioactive bitter substances in our diet, it is possible that gastrointestinal T2Rs evolved to perceive bitter‐tasting phytochemicals in anticipation of the incoming carbohydrate load, resulting in rapid changes in the gastrointestinal glucose absorption and utilization by paracrine signaling. Using a cell culture model of the small intestine, we confirmed that multiple classes of bitter phytochemicals activate bitter receptor signaling and suppress uptake of glucose from the intestinal lumen, mediated in part by cholecystokinin (CCK). Additionally, treatments with bitter extracts from chicory and other edible plants affected the PLC/PKC signaling pathway downstream of T2Rs, thus controlling biomarkers of immune and bioenergetic responses in the intestine. As alterations in normal glucose transport are strongly associated with multiple metabolic pathologies including obesity, diabetes, and cancer, these finding support the use of bioactive bitter phytochemicals to control postprandial glycaemia and reduce caloric intake in high‐risk populations in clinical and community settings. Support or Funding Information This work was supported in part by NCSU Research and Innovation grant 2012‐2246 (SK); NCSU Office of International Affairs grant 2013‐1705 (SK); Plants for Human Health Institute grant 429350‐42567 (SK); and Cell Culture and Phenotyping Core of the Plants for Human Health Institute, NC State University.