If the link bears out, CD36 would allow fat to join the five previously identified tastes that govern the experience of food: bitter, salty, sweet, sour and "umami," or savoriness (like the meaty goodness of soup stock).
Researchers have long debated whether a sensor for fat existed, given that many animals display an innate attraction to fats. To determine whether CD36--a protein expressed in the taste buds--might be the culprit, a team at the University of Bourgogne devised an experiment using mice that had been genetically modified to lack CD36. These mice, along with a group of wild mice were fed two solutions: one laced with fat and one containing xanthan gum to mimic fat's mouthfeel.
Wild mice craved the fatty solution. The mice missing CD36, in contrast, showed no preference either way. In addition, neither group exhibited a change in either their desire for sugar or aversion to quinine, indicating that CD36's effect was limited to fats.
Furthermore, removal of the CD36 gene in rats prevented their digestive tracts from preparing the various gastric juices necessary to digest fat. "Because expression of CD36 within the oral cavity and its effect on digestive secretions are conserved in mice and rats, it is likely that CD36 performs a basic function in the taste bud cells," Philippe Besnard and his fellow authors conclude in the current issue of the Journal of Clinical Investigation.
The authors caution, however, that further studies are needed to determine whether CD36 is indeed the elusive fat sensor, how it signals fat to the taste bud, and, ultimately, why that prompts craving. "The sensory experience of food can be a primary reinforcer of intake," writes Nada Abumrad of Washington University in an accompanying commentary. "As more is learned about the specificity and mechanism of this receptor's function, it may be possible to devise strategies to treat some forms of obesity."