ICEECE2012 Symposia The gut nutrient sensing in energy metabolism (3 abstracts)
Monell Chemical Senses Center, Philadelphia, Pennsylvania, USA.
We have found that many of the receptors and downstream signalling elements involved in taste detection and transduction are expressed also in intestinal hormone producing (endocrine) cells where they underlie key chemosensory functions of the gut. In one example of gastrointestinal chemosensation it is known that glucose given orally, but not systemically, induces secretion of the incretin hormone glucagon like peptide-1 (GLP-1), which in turn regulates insulin secretion and glucose homeostasis. We have found that intestinal endocrine cells express sweet taste receptors, the taste G-protein gustducin, and several other taste transduction elements. Knockout mice lacking gustducin or the sweet taste receptor subunit T1R3 have deficiencies in secretion of GLP-1 and in the regulation of plasma levels of insulin and glucose. We have studied intestinal cell lines that express gustducin, taste receptors and other taste signaling elements to identify the roles of these taste proteins in regulating GLP-1 hormone release. In another example of gastrointestinal chemosensation we have found that endocrine cells of the pancreas express multiple taste proteins that are involved in regulating insulin release. Furthermore, taste cells of the oral cavity express GLP-1, other gut hormones and the insulin receptor. Most recently, we have identified intestinal-type glucose transporters and pancreatic-type ATP-gated K+ channels (K-ATP metabolic sensors) as being present in taste cells and potentially functioning in the detection of the sweet taste of sugars. In sum these studies point out similarities in gustation and gut chemosensation and indicate the importance of taste cells of the gut and endocrine cells of the tongue in coordinating the bodys hormone responses to regulate glucose homeostasis.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This work was supported, however funding details are unavailable.