Curiosity about the cat has finally paid off with a scientific explanation for felines' enigmatic indifference to sweets.
Researchers, pet owners and cat chow manufacturers have long recognized that cats, in stark contrast to their canine counterparts, show no particular attraction to sugar. Having sampled two dishes of water, one spiked with sugar and the other not, a cat is as likely to lap from one as the other.
But why? Until now, scientists have not known whether cats simply lack the lingual apparatus to detect sugar; or have functional sugar detectors on their tongues but faulty wiring from their taste buds to the brain; or -- as some might presume -- are simply too snooty to admit to such a common craving.
Now researchers studying the DNA of house cats, tigers and cheetahs have settled the question: Cats both large and small harbor a genetic mutation that renders the sugar detectors on their taste buds inoperative.
"We have found a simple but elegant explanation for their behavior," said Joseph G. Brand of the Monell Chemical Senses Center in Philadelphia, who with co-worker Xia Li led the study, published yesterday in the journal PLoS Genetics.
The work fills a gap in scientists' understanding of the evolution of cats, whose indifference to sugar -- a rare trait among mammals -- complements their complete dietary dependence on meat. In humans and other animals that depend on starches and ripe fruits for a sizable part of their nutrition, the ability to detect sugars is crucial.
"This discovery highlights how a species can manage to do without an entire taste modality if it has an ecological niche that will support that lifestyle," said Charles Zuker, a Howard Hughes Medical Institute investigator at the University of California at San Diego who co-discovered the receptor for sweetness in 2001.
The research also offers a glimpse into how animals other than humans experience the world.
After all, an organism's conception of reality is completely dependent on its senses, such as taste, vision and hearing, said Nick Ryba, a National Institutes of Health researcher who co-discovered the sweetness receptor with Zuker. Yet each kind of animal perceives but a small part of the overall sensory universe.
People cannot see infrared light, for example, a part of the visual spectrum that colors some insects' worlds, and they cannot hear the high-frequency sounds to which dogs respond. Dogs, on the other hand, are red-green colorblind. And some animals, such as blue crabs, can taste nutrients called purines that other creatures have no way of sensing.
Such differences go a long way toward explaining why various creatures behave and live as they do.
"If you think about it, what we actually perceive is not in fact reality at all," Ryba said. "It's really something that our brain constructs out of the information that it receives through our sense organs."
Brand, who has two cats, said he could not say for sure how a cat's overall nature might be affected by never experiencing sweetness. But it may not be a coincidence, he said half-jokingly, that the dominant behavioral characteristics of a cat are that "it sleeps a lot and it's cranky."
Human taste buds contain cells with five kinds of "receptors," each specifically responsive to one of five tastes: salty, bitter, sweet, sour and umami (a taste imparted by amino acids, including flavor enhancer monosodium glutamate).
The sweetness receptor consists of two different proteins attached to each other on the surface of a cell. The two are manufactured under the direction of two genes, then embrace to make a single receptor that fires a nerve signal to the brain when sugar is present.
In the new study, the researchers collected DNA from six house cats, all of them pets of scientists at Monell. They analyzed the sequence of genetic "letters" in the two genes encoding the sweetness receptor's two proteins.
They found that one of those genes, called Tas1r2, is missing a stretch of 247 letters -- a deletion that prevents the gene from making a proper protein. With only one of the two crucial proteins, the cats have no way to taste sweetness.
The researchers found the same deletion in tiger and cheetah DNA, suggesting the mutation occurred in a common ancestor early in feline evolution. Follow-up studies are now underway using DNA from a civet, mongoose and hyena, all of which evolved from the same common ancestor. The goal is to pinpoint when in feline evolution the deletion occurred.
It is not clear whether the cat's loss of its sense of sweetness led it to pursue an all-meat diet or, as Brand and others suspect, cats were already fully carnivorous -- in which case the loss of an affinity for sweets would hardly have mattered to them.
Also unclear is why some cats at least dabble in sweets, licking the occasional melon ball, for example. But the experience of flavor is only partly due to taste and is largely a function of a food's smell, Brand noted, suggesting that cats are probably attracted to either the smell of some sweets or the salts or amino acids that are also present.
Because the Tas1r2 deletion is a big one, it is unlikely any cat would be born with a spontaneously corrected version of the gene. One of the cats in the Monell experiment was crazy about marshmallows, Brand said, briefly raising hopes that it might be a rare mutant. But DNA tests proved the cat was no different than the others.
"Whatever this cat finds attractive in marshmallows, it's not sugar," Brand said.
Zuker said he has been contacted by many people who suspect their sweet receptors are nonfunctional. "They say they don't really know what 'sweet' means," he said.
But as far as he knows, none has had a DNA test.
And no one knows if those people sleep a lot or are cranky.