Cornell University food scientists have discovered that when mice are fed a high-fat diet and become obese, they lose nearly 25% of their tongue’s taste buds. As a result, the mice—through an obesity-triggered metabolic malfunction—may be encouraged to eat more food.

“This is a potential human mechanism for getting fat,” said senior author Robin Dando, assistant professor of food science, in a new study in PLOS Biology, March 20.

“Evidence suggests that obesity from an unhealthy diet results in a powerful [metabolic] inflammatory response,” Dando said. “In mice, this response disrupts the balance of taste bud renewal, reducing how many mature taste buds these mice have. This research provides new clues about how humans might become obese and suggests a novel approach to combating obesity—looking at the taste bud itself.”

The researchers tested normal and obesity-resistant mice. On a high-fat diet, the normal mice gained about 30% of their base body weight. The scientists found that obesity-resistant mice—consuming the same, unhealthy diet as other mice in the litter—didn’t gain nearly as much weight, and along with this had normal taste bud abundance, suggesting that taste bud loss is a metabolic response to obesity, rather than a result of exposure to fat.

In past research, obese people have reported a weakened sense of taste and thus may be driven to consume more calories.

“Combining those results with this new work, it’s an interesting takeaway. Our obese mice would not be getting as much input from taste. If the same taste loss happens in obese humans, it’s plausible these people would be driven to eat more, or at least eat a more intensely tasting version of whatever they were eating,” Dando said.

In humans, taste buds contain receptors that report when a food is bitter, salty, sweet, sour, or umami. A normal tongue has about 10,000 taste buds, the cells of which are renewed once or twice a month. Obesity, through a weakened metabolism, wrecks the renewal process and reduces the number of taste buds—keeping a human in an obesity cycle.