Abstract
Thiamine and quinine are popular bitter substances and their physiological effects have been studied; however, their impact on digestion remains unknown. Here, the physiological effects of thiamine and quinine was investigated for in vitro contraction of mouse ileum. Acetylcholine stimulates autonomous contraction of mouse ileum in a dose-dependent manner. The effect of Acetylcholine for contraction of ileum was partly suppressed by the adrenaline administration. Upon simultaneous treatment of the ileum by acetylcholine, thiamine, and quinine decreased the maximum contraction. The period till half maximum contraction was prolonged by the presence of thiamine and quinine but not by adrenaline. Because a physiological effect of thiamine and quinine was observed on acetylcholine-induced contraction of the ileum, the repertoire of human bitter taste receptors, TAS2R-1, -4, -7, -10, -14, -31, -39, -40, -43, and -46, were investigated to which thiamine and quinine may bind. These human bitter taste receptors were further analyzed among the database for mouse homologs using evolutionally conserved amino acid sequences. The only bitter receptor for both thiamine and quinine was TAS2R-39, the homology of TAS2R-139 to human TAS2R-39 was 74%. Importantly, the homology of mouse TAS2R-119 to human TAS2R-1 which interact with thiamine was 91%, and that of TAS2R-130 to human TAS2R-7 that interact with quinine was 81%. The present study indicated that thiamine and quinine changed the early phase of contraction of ileum in mice and suggested that TAS2R119 and TAS2R130 expressed in mouse enteroendocrine cells to modify the physiological effects of thiamine and quinine on the acetylcholine-induced contraction of the ileum.
Highlights
Taste is one of the main chemosensory systems required for survival; it is essential to identify chemical substances in food so as to avoid toxic substances or to intake favorable nutritional sources [1,2,3]
Bitter, or umami taste bind to specific receptors and modify certain cell functions via taste receptors coupled with calcium-signaling molecules (TRCSMs), such as phospholipase C-β2, gustducin, and inositol 1,4,5-triphosphate [3,4,5,6,7,8,9]
It has previously been reported that caffeine binds to several type 2 taste receptors (TAS2Rs), which are known to detect bitter taste, and caffeine-binding TAS2Rs have been shown to be reactive to other bitter substances [30]
Summary
Taste is one of the main chemosensory systems required for survival; it is essential to identify chemical substances in food so as to avoid toxic substances or to intake favorable nutritional sources [1,2,3]. ICCs play a major role in intestinal contraction without the involvement of motor neurons, hormones, or inflammatory mediators, and have been suggested to be modulated by several nutrients [23,24,25,26]. Another previous study reported an inhibitory action of caffeine on the smooth muscle contraction [27]. The effects of several bitter substances and TAS2Rs were investigated in the contraction of the mouse ileum
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