Domestic cats (Felis silvestris catus) (herein referred to as “cats”) are neither attracted to, nor show avoidance of the taste of sweet carbohydrates and high-intensity sweeteners (1-3), yet they do show a preference for selected amino acids (4), and avoid stimuli that taste either bitter or very sour to humans (1,4). Consistent with this behavioral evidence, recordings from cat taste nerve fibers and from units of the geniculate ganglion innervating taste cells demonstrated responses to salty, sour, and bitter stimuli as well as to amino acids and nucleotides, but showed no response to sucrose and several other sugars (4-11). The sense of taste in cats appears similar to that of other mammals with the exception of an inability to taste sweet stimuli.
Because only the sweet taste modality appears absent, we postulated that the defect in cats (and likely in other obligate carnivores of Felidae) lay at the receptor step, subtending this modality. The possible defects at the molecular level could range from a single to a few amino acid substitutions, such as is found between sweet “taster” and “nontaster” strains of mice (12-14), to more radical mechanisms, such as an unexpressed pseudogene.
To distinguish among these possibilities, we identified the DNA sequences and examined the structures of the 2 known genes Tas1r2 and Tas1r3 that encode the sweet taste receptor heteromer T1R2/T1R3 in other mammals. We compared these with the sequence and structure of the same genes in dogs, humans, mice and rats, all species that respond to sweet stimuli.