Sugar receptors previously thought to exist only in the gut have been identified on sweet taste cells on the tongues of mice, possibly explaining why salt enhances sweetness intensity, according to new research.
The study, published in Proceedings of the National Academy of Sciences, found that glucose transporters (GLUTs) and sodium-dependent glucose transporter (SGLT1), sweet receptors that were previously believed to only be found in the intestine and pancreas, are also expressed in oral taste cells of mice.
The researchers, from the Monell Chemical Senses Center, USA, said that the findings increase the knowledge of how taste cells detect sugars and may explain another mystery of sweet taste; why a pinch of salt sometimes tastes sweet, and why salt added to baked goods boosts sweet taste.
The researchers, led by senior author Dr Robert Margolskee of the Monell Center, added that “taste cell-expressed glucose sensors and potassium-ATP channels may serve as mediators of … T1r-independent sweet taste.”
The authors explained that it has long been known that the T1r2+T1r3 receptor is the primary mechanism to detect sweet compounds, including sugars and artificial sweeteners.
However, Margolskee and his colleagues noted that some aspects of sweet taste cannot be fully explained by activation of the T1r2+T1r3 receptor.
For example, they noted that the receptor T1r2+T1r3 contains two subunits that must join together for it to work properly; but previous work from Margolskee's team has found that mice engineered to be missing the T1r3 subunit are still able to taste sugar.
Using advanced molecular and cellular techniques to test for these sweet receptors in taste cells, the Monell team discovered that several glucose receptor/transporter proteins found in other tissues (including GLUT2, GLUT4, GLUT8, and GLUT9), a sodium–glucose co-transporter (SGLT1), and two components of the ATP-gated potassium (potassium-ATP) blood-sugar metabolic sensor were expressed in oral taste cells of mice.
The researchers found that that in particular, GLUT4, SGLT1, and SUR1 were expressed preferentially in T1r3-positive, sweet taste cells. They also determined that nearly 20 per cent of the total sweet receptor’s sensory output in mouse taste cells originated from potassium-ATP channels.
The authors explained that the presence of the SGLT1 receptor (which transports sugars into cells only when sodium is present) on oral sweet taste cells may explain why taste sweet perceptions can be more when salt is present in food.
Margolskee and his colleagues also said that that potassium-ATP may function in sweet taste cells to modulate taste cell sensitivity to sugars according to metabolic needs.
“Sweet taste cells have turned out to be quite complex. The presence of the potassium-ATP channel suggests that taste cells may play a role in regulating our sensitivity to sweet taste under different nutritional conditions,” said Dr Karen Yee, a cellular physiologist at Monell, and first author of the research.
Source: Proceedings of the National Academy of Sciences (PNAS)
Published online ahead of print, doi: 10.1073/pnas.1100495108
“Glucose transporters and ATP-gated K+ (KATP) metabolic sensors are present in type 1 taste receptor 3 (T1r3)-expressing taste cells”
Authors: K.K. Yee, S.K. Sukumaran, R. Kotha, T.A. Gilbertson, R.F. Margolskee