Despite evidence that the ability to taste is weakened by obesity and can be rescued with weight loss intervention, few studies have investigated the molecular effects of obesity on the taste system
Taste bud cells undergo continual turnover even in adulthood, exhibiting an average life span of only a few weeks, tightly controlled by a balance of proliferation and cell death. Recent data reveal that an acute inflammation event can alter this balance. We demonstrate that chronic low-grade inflammation brought on by obesity reduces the number of taste buds in gustatory tissues of mice—and is likely the cause of taste dysfunction seen in obese populations—by upsetting this balance of renewal and cell death.
Taste buds operate not only as sensors of essential nutrients but can also trigger powerful central reward from the consumption of hedonically pleasing food. Obese individuals have been reported to display a weakened sense of taste and thus may be driven to consume more calories to attain such reward. Here, we have analyzed the effects of obesity on taste buds and demonstrate that mice consuming a high-fat diet quickly become obese and display a pronounced loss of taste buds when compared to littermates sustained on a healthy diet. When the inflammatory response is impeded via genetic manipulation, we observe that mice no longer suffer taste loss, suggesting that taste dysfunction in obesity is a result of systemic inflammation. We also find that obesity-resistant mice consuming the same unhealthy diet have no change in the taste bud abundance, confirming that taste loss is a metabolic consequence of the obese state rather than a response to oral exposure to fat. Our results validate a role for taste in the genesis of obesity and suggest a novel direction in the treatment of obesity.
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