Taste receptor downregulation in diet-induced obesity reveals circumvallate papillae-specific taste-inflammatory networks.

INTRODUCTION

Beyond their role in chemosensory perception, taste receptors function as metabolic regulators extra-orally. While decreased taste receptor expression in gustatory tissue is linked to obesity-associated inflammation, we tested the hypothesis that taste receptor-inflammation interactions extend to extra-oral contexts.

METHODS

Obesity-associated metabolic syndrome-like phenotype was induced in female C57BL/6 mice by administration of a cafeteria diet for 18 weeks. The controls consumed a standard diet. Gene-expression levels of Tas1r2, Tas1r3, CD36, Ffar1, GPR84 and Ffar4 were analyzed in circumvallate papillae, lower jejunum, stomach and spleen using RT-qPCR. The number and area of fungiform papillae were assessed on the anterior tongue. Correlation network connectivity for taste receptor expression and fungiform papillae markers with inflammatory and cardiometabolic risk markers was calculated tissue-specifically.

RESULTS AND DISCUSSION: The cafeteria diet induced obesity, metabolic dysfunction, and systemic inflammation. Additionally, number and area of fungiform papillae were reduced, and Tas1r2, CD36, Ffar1 and GPR84 were downregulated in circumvallate papillae, whereas in jejunum only CD36, Ffar1, and GPR84 were downregulated following cafeteria diet. Gustatory sweet and fatty acid receptor expression correlated with dietary intake patterns. Exploratory network analysis indicated tissue-specific correlation patterns, with taste receptor-inflammation crosstalk predominantly appearing orally. In contrast, extra-oral sweet and fatty acid receptor expression showed weaker or absent correlations with systemic inflammatory markers under the conditions tested.