With many of us still recovering from the Easter chocolate frenzy, it is timely to consider the processes that underlie our partiality to sweet foods and the reasons why some people are more susceptible to their charms than others. Indeed, the 'sweet tooth' phenomenon is not confined to humans; it has long been known that different strains of mice vary in their preference for sweet-tasting substances. A candidate locus for sweet detection — Sac — has been identified in mice, but not in humans, and no specific sweet-taste receptors were known until recently. However, as reported in Nature Genetics and Nature Neuroscience, two research groups have now independently identified what appears to be the first mammalian sweet taste receptor.

Five different types of tastant can be distinguished by mammals: sweet, sour, bitter, salty and glutamate (umami). The receptors for salty and sour tastes have been identified as ion channels, whereas other tastes are believed to be transduced by G-protein-coupled receptors (GPCRs). To identify sweet taste receptors, Max et al. and Montmayeur et al. searched the human genome databases for new GPCR genes that map to, or near to, the human equivalent of the mouse Sac locus. Both teams cloned the mouse homologue of one gene that fulfils these criteria, and the protein that it encodes was named T1r3.

Mouse strains were classed as 'tasters' (those that preferred water containing sucrose or saccharin to plain water) and 'non-tasters' (those that showed little or no preference). Both groups showed that there are allelic differences at the T1r3 locus between tasters and non-tasters. The specific expression of its mRNA in the papillae (taste buds) of the tongue is also consistent with T1r3 being a taste receptor. Interestingly, in many taste cells, T1r3 is co-expressed with the related GPCR T1r2, which has also been implicated in taste reception. There is increasing evidence that dimerization is important for GPCR function, and T1r3 could form heterodimers with T1r2 (and/or other as yet unidentified GPCRs), thereby increasing the repertoire of receptors to allow for detection of different sweet tastants. Max et al. propose that one of the mutations seen in the non-taster allele might introduce a glycosylation site that inhibits dimerization.

With the incidence of obesity on the rise both in the United Kingdom and the United States, understanding the mechanisms underlying our predilection for particular foods inevitably becomes linked to human health issues. Max et al. predict that one spin-off from their research might be the design of better artificial sweeteners, which will hopefully help us to satisfy our cravings for sugar without piling on the calories. Also, by studying those people who seem to have been born without a sweet tooth, it might be possible to develop strategies to make sweetness less appealing.