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A study by Andrew Kaufman, Robin Dando, and colleagues at Cornell University shows that inflammation, driven by obesity, reduces the number of taste buds on the tongues of mice. A taste bud comprises of approximately 70 to 100 cells of three major types, each with different roles in sensing the five primary tastes-salt, sweet, bitter, sour, and umami. Taste bud cells turn over quickly, with an average lifespan of just 10 days. Weight gain can reduce sensitivity to the taste of food.
The authors fed some mice a normal diet made up of 14% fat, or an obesogenic diet containing 58% fat to detect changes in taste buds. After some weeks, the mice fed the obesogenic diet weigh about one-third more than those receiving normal food. But the obese mice had about 25% fewer taste buds than the lean mice, with no change in the average size or the distribution of the three cell types within individual buds.
The turnover of taste bud cells normally arises from a balanced combination of programmed cell death-apoptosis and generation of new cells from special progenitor cells. However, the researchers discovered that the rate of apoptosis increased in obese mice, whereas the number of taste bud progenitor cells in the tongue declined, showing the net decline in the number of taste buds. Mice that were genetically resistant to becoming obese did not show these effects, after eating a high-fat diet.
Obesity is associated with a chronic state of low-grade inflammation, and adipose tissue produces pro-inflammatory cytokines – molecules that serve as signals between cells – including one called TNF-alpha. High-fat diet increased the level of TNF-alpha surrounding the taste buds; however mice that were genetically incapable of making TNF-alpha had no reduction in taste buds, despite gaining weight. Injecting TNF-alpha directly into the tongue of lean mice led to a reduction in taste buds, despite the low level of body fat.
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