|Budget Amount *help
¥112,450,000 (Direct Cost: ¥86,500,000、Indirect Cost: ¥25,950,000)
Fiscal Year 2010: ¥17,290,000 (Direct Cost: ¥13,300,000、Indirect Cost: ¥3,990,000)
Fiscal Year 2009: ¥16,770,000 (Direct Cost: ¥12,900,000、Indirect Cost: ¥3,870,000)
Fiscal Year 2008: ¥16,770,000 (Direct Cost: ¥12,900,000、Indirect Cost: ¥3,870,000)
Fiscal Year 2007: ¥17,680,000 (Direct Cost: ¥13,600,000、Indirect Cost: ¥4,080,000)
Fiscal Year 2006: ¥43,940,000 (Direct Cost: ¥33,800,000、Indirect Cost: ¥10,140,000)
Reception and modulation of taste signals and their roles in the regulation of food intake are investigated by examining taste cell, nerve and behavioral responses to various taste compounds. The results showed that sweet taste signal is initiated from a particular group of taste cells expressing T1r2/T1r3 sweet receptors and is transmitted to its corresponding group of nerve fibers through ATP release. Sweet taste sensitivity is inhibited by leptin, a satiety hormone, of which plasma level has a diurnal variation. Sweet taste thresholds also show diurnal variation that is parallel with that of plasma leptin levels. This synchronization, however, is not evident in obese subjects. Analyses on single nucleotide polymorphisms of umami receptor genes indicate existence of multiple receptors in umami perception in humans. These results provide new findings in the taste receptor and transduction mechanisms and new insights for potential roles of peripheral taste signal in the control for food intake, of which abnormality may possibly lead to the obesity.