Inflammation arising from obesity reduces taste bud abundance and inhibits renewal.

Andrew Kaufman,Anna Koh,Robin Dando,Ezen Choo,Ken Cadwell

doi:10.1371/journal.pbio.2001959

Abstract

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.

Highlights

Obesity is one of the world’s most prevalent public health issues, affecting over one-third of United States citizens [1] and is associated with increased mortality, along with various comorbidities, including cardiovascular disease, diabetes, stroke, and cancer [2]
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

Summary

Introduction

Obesity is one of the world’s most prevalent public health issues, affecting over one-third of United States citizens [1] and is associated with increased mortality, along with various comorbidities, including cardiovascular disease, diabetes, stroke, and cancer [2]. Earlier reports suggest little to no effect of BMI on taste sensitivity [4,5] These studies tested detection thresholds for sweet stimuli in obese and normal-weight humans but failed to take into account individual variation in the perception of suprathreshold stimuli. Researchers have explored the association between high BMI and decreased dopamine signaling from food intake, suggesting that the obese and overweight seek out more palatable foods to compensate for depressed reward [12,13]. Weight loss interventions, both gradual and acute (i.e., via bariatric surgery), have proven to alleviate obesity-related alterations in taste function, suggesting a bidirectional relationship between adiposity and taste. Various groups studying functional responses from taste buds of obese rodents have noted an altered response to sweet and fat stimuli [22,23,24], often accompanied by a decreased behavioral response

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