Molecular and Neural Mechanisms for Detection, Transmission and Modulation of taste signals derived from the oral cavity and gut
Description: The present study investigated reception and modulation of taste signals in the oral cavity and gut and their roles in the regulation of food intake. The results showed that sweet sensitivity in lean mice was chronically inhibited by leptin, a satiety hormone, whereas in obese mice no such leptin effect was evident and instead their sweet sensitivities were enhanced by endocannabinoids, orexigenic mediators. This leptin/endocannabinoid reciprocal modulation of sweet sensitivity was also found in gut endocrine STC-1 cells. Conversely, GLP-1, a gut peptide hormone, was found to be involved in sweet signal transmission from taste cells to brain in mice and genetic variations of GLP-1 receptor gene link with sweet recognition thresholds in human. These results provide new line of evidences in taste receptor mechanisms in the oral cavity and gut and new insights for potential roles of peripheral taste signals in control for food intake, of which abnormality may possibly lead to the obesity.
Amount: ¥47,190,000
Funding type: research
Funder scheme: Grant-in-Aid for Scientific Research (A)
Start date: 2011-04-01
End date: 2014-03-31
Investigator: Yuzo NINOMIYA
Institution: Kyushu University
Funded outputs count: 17
Funder award ID: 23249081
OpenAlex ID: G831799783