Stimulation of the fatty acid transporter molecule CD36 with long-chain fatty acids in mouse taste buds induces changes in feeding behavior and gastric physiology, suggesting CD36 could serve as a taste receptor for fat in rodents. The finding, reported in the November 1 issue of the
The sense of taste is conventionally depicted as five canonical modalities – sweet, salt, sour, bitter, and "umami" (L-amino acid, described as meaty or savory). Researchers have also recognized receptors for other gustatory stimuli, such as menthol and capsaicin, or chilli.
Still, animals clearly are also drawn to fat, and evidence suggests that this attraction may stem from fat's taste, not just its texture. Philippe Besnard, who led the study at the University of Bourgogne in Dijon, France, told
"Historically, it's always been thought that the most salient cue for fat is its texture," said taste researcher Tim Gilbertson of Utah State University in Logan, who was not involved in the study. "We are moving more toward the idea that there may be both taste and texture involved in fat perception."
According to Besnard, triglycerides, not fatty acids, comprise the bulk of dietary lipids. Several lines of evidence suggest that CD36 -- an integral membrane glycoprotein that facilitates fatty acid uptake in a range of tissues – may be a promising candidate for a lipid taste receptor, he noted. CD36 is expressed on rats' tongues, for example, and applying long-chain fatty acids (LCFAs) to rat taste bud cells inhibits delayed-rectifying K+ channels, implicated in the transduction pathways of a variety of taste stimuli.
Indeed, during the study, Besnard and his team found that, unlike their wild-type counterparts, CD36-null mice show no preference for fatty foods. Stimulating CD36 also appears to elicit physiological changes that prime the digestive system to anticipate a fat-rich meal. When the researchers applied LCFAs to the tongues of wild-type rats and mice with an esophageal ligation to prevent food reaching the intestine, they recorded a rapid rise in pancreatobiliary secretions. "CD36 gene inactivation in the mouse fully abolishes these physiological changes," said Bresnard.
Furthermore, Besnard's team located CD36-expressing cells on a region of the tongue that exposes them to high levels of lingual lipase, which generates fatty acids from triglycerides. "Such an anatomical design may be sufficient to generate a LCFA stimulus in taste receptor cells," noted Besnard.
He suggested that a taste modality for lipids "might have an important impact on energy balance and health." Indeed, in an accompanying commentary, Nada Abumrad of the Washington University School of Medicine, St Louis, argues that the finding might shed light on the addictive quality of lipids, given the hyperphagic effects of a high-fat diet. "If we increase fatty acids over the long term, does that receptor become upregulated?" she told
Gilbertson noted that humans also possess CD36, although he is not aware of evidence that it is expressed in taste buds. If so, he suggested that Bresnard's work might inform the development of fat substitutes that imitate both the texture and the taste of lipids. "Some of those on the market that have been designed to mimic the textural properties have not been hits with the consumer," he told
Besnard said that his team is now developing rodent models that overexpress or lack CD36 only in the taste buds, in order to explore the role of the receptor in obesity.