Taste buds comprise of about 50 to 100 cells in 3 types each playing different roles of the primary tastes which are sweet, umami, sour, salt, and butter. Taste bud cells have a quick turn over with the average lifespan of 10 days. Taste bud cells turn over typically comes from a balanced combination of programmed apoptosis cell death with new cells generated from progenitor cells. To investigate changes in taste buds with obesity mice were fed either a normal diet consisting of 14% fat, or an 58% fat obesogenic diet.
Researchers observed that over 8 weeks the high fat diet animals weighed one third more, and these animals had 25% less taste buds, with no other changes in average size or distribution of the 3 cell types within the individual buds. The rate of apoptosis was increased in the obese animals, and the number of taste bud progenitor cells in the tongue decreased. Animals which were genetically resistant to becoming obese were not observed to display these effects even when fed high fat diets, which implies that the changes are not due to fat consumption but rather accumulations of fatty adipose tissues.
Obesity is associated with chronic low grade inflammation as adipose tissue produces pro-inflammatory cytokines including one called TNF-alpha. Levels of TNF-alpha surrounding the taste buds were found to be increased in the animals on high fat diets, with the animals which were genetically unable to make TNF-alpha having no reduction in taste buds even with weight gain. Injecting TNF-alpha directly into the tongue of lean animals led to taste bud decreases even with low levels of body fat.
Researchers suggest that data of gross adiposity stemming from exposure to high fat diets is associated with low grade inflammatory response causing disruption in balancing mechanisms involved in taste bud renewal and maintenance, results may be useful towards developing novel therapeutic strategies for treating taste bud dysfunction in obese patients
