Sweet taste receptors

An alternative view (123) is that no single model can adequately explain why any given compound is sweet. This hypothesis derives from several features. First, there is the observation that all carbohydrates having a critical ratio of OH to C are sweet tasting. In other words, there are no stmctural constraints to the sweetness of carbohydrates. Second, not all sweeteners can be fit to the same SAR model. Rather, some fit one, others fit another. Third, studies on the transduction mechanisms of sweetness suggest more than a single mechanism for sweet taste, implying multiple receptors for sweeteners. 

Lactisole [13794-15-5] the sodium salt of racemic 2(4-methoxyphenoxy)propionic acid, is a sweet-taste inhibitor marketed by Domino Sugar. It was affirmed as a GRAS flavor (FEMA no. 3773). At a concentration of 100 to 150 ppm, lactisole strongly reduces or eliminates the sweet taste of a 10% sugar solution. This inhibition appears to be receptor-related because lactisole also inhibits the sweet taste of aspartame. The 5 -( —)-enantiomer [4276-74-8] (38), isolated from roasted coffee beans, is the active isomer the i -(+)-enantiomer is inert (127). 

The theories that attempt to describe the initial event in sweet-taste stimulation will be discussed, as will some of the practical attempts to isolate sweet-receptor molecules. Relevant, behavioral data will be examined, particularly where the effects of molecular structure on behavior responses are being evaluated. 

That the initial event of taste stimulation takes place on the cell surface of the taste receptor is now universally accepted. In addition, accumulated evidence strongly suggests that taste-bud stimulation is extracellular in nature. For example, (1) the sweet-taste response is both rapid and reversible, (2) the intensely sweet proteins monellin" and thaumatin could not possibly penetrate the cell, because of their size, and (3) miraculin, the taste-modifying glycoprotein, having a molecular weight of 44,000 would also be too large to penetrate the taste cell. ... 

There is little doubt that Shallenberger s AH,B hypothesis is the most plausible concept in the explanation of the initial stimulation of the sweet-taste receptor. However, it was unfortunate that the evidence was accrued largely with the aid of reducing sugars, which, in solution, equilibrate between many isomers, so that it is not possible to relate total gustatory response to any one particular stereochemical structure It is also not... 

However, the model is defined such that the terms ir, a, fi, and a may all be measures of different types of receptor-sweetener binding. These all reflect the probability of that event s occurring, while, at the same time, the probability of the sweetener s reaching its receptor, and that of the receptor complex s undergoing the response-eliciting reaction, may both be unity The sole criterion for the sweet-taste response would thus require the formation of the proper sweetener-receptor complex. The validity of such a hypothesis has yet to be proved. " ... 

The AH unit was assigned to the carboxyl group, as the sweet taste of compounds 2 and 3 in Table XXIVa is lost when the carboxyl group is absent or when it is converted into the methyl ester (compound 4 in Table XXIVa). It was suggested " that this group mainly interacts with its counterpart on the receptor by ionic interaction. The absence of sweet taste... 

Montmayeur, J. P. et al. A candidate taste receptor gene near a sweet taste locus. Nat. Neurosci. 4 492-498, 2001. 

Nelson, G. etal. Mammalian sweet taste receptors. Cell 106 381-390, 2001. 

Kitagawa, M. et al. Molecular genetic identification of a candidate receptor gene for sweet taste. Biochem. Biophys. Res. Commun. 283 236-242, 2001. 

Sweet taste receptor, 24 246-247 identification of, 24 248 Sweet-taste transduction mechanisms,... 

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