Mammalian sweet perception depends on a receptor assembled from two proteins, T1R2 and T1R3. In cats the gene encoding T1R2 carries deletions that prevent a working protein from being made, so the receptor pair cannot form. The defect has been found across the cat family, from house cats to tigers, indicating it arose early in feline evolution.
This is a plausible consequence of hypercarnivory rather than its cause. A lineage that obtains almost no carbohydrate from its diet loses little by letting a sugar detector decay. Cats also have a reduced repertoire of bitter receptors relative to omnivores, and they are unusually sensitive to the taste of certain amino acids and nucleotides that signal meat.
Cats that appear to enjoy ice cream or sweetened foods are responding to fat, dairy protein or texture, not to sugar. The distinction matters clinically: because sweetness does not register, sugar in a cat's food carries no palatability benefit while still contributing calories a strict carnivore is poorly equipped to process.

