Bitter sensing in the gastrointestinal tract (#223)
Chemosensory systems in the gastrointestinal (GI) tract play an important role in monitoring the composition of gut luminal contents during digestion and subsequent modulation of gut function and feeding behaviour. Bitter food components have been implicated in the post-ingestive modulation of satiety and represent a possible mechanism for the development of enhanced appetite control foods. In humans, bitter compounds are detected by a family of 25 known bitter taste receptors (TAS2Rs) expressed in a range of cell types including enteroendocrine cells of the gastrointestinal tract mucosa. TAS2R activation by bitter food components stimulates the release from enteroendocrine cells of gut peptide hormones involved in the regulation of GI function and appetite e.g. Cholecystokinin (CCK).
We have examined the expression of specific TAS2Rs in human gastric, small intestinal and colonic tissue mRNA libraries and validated an in vitro human enteroendocrine I-cell model (Hutu-80) using a variety of known TAS2R bitter agonists.
We show that mRNAs for bitter taste receptors are expressed in human gastric, small intestinal and colonic tissue as well as the Hutu-80 cell-line. In addition, Hutu-80 cells respond to a subset of known bitter agonists via a G-protein coupled phospholipase C mediated pathway, elevated cytoplasmic calcium concentrations and subsequent release of CCK.
In conclusion, the capability to sense luminal bitter compounds may occur throughout the GI tract. However, not all known lingual bitter agonists stimulate hormone secretion in Hutu-80 cells, suggesting key differences between lingual and GI bitter sensing that may have important implications for design of functional foods to modulate appetite through bitter sensing.