Frontiers in nutrition · 2026
Sensory signaling mediates the systemic metabolic and neurological effects of epigallocatechin gallate.
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Yoshida Yamato, Iida Naoki, Iwasa Kenshin, Saito Akuru, Aso Kenta, Fujii Yasuyuki, Modafferi Sergio, Calabrese Vittorio, Ohmoto Makoto, Abe Keiko, Osakabe Naomi
Аннотация
BACKGROUND: Epigallocatechin gallate (EGCG), the primary green tea flavanol, is renowned for its diverse health benefits; however, its low systemic bioavailability presents a long-standing paradox in nutritional science. We hypothesized that EGCG exerts its physiological effects via oral chemosensory signaling pathways, independent of intestinal absorption.
METHODS: This study utilized wild-type and Skn-1a-/- mice (lacking bitter taste signaling) to evaluate acute metabolic responses. Furthermore, a chronic study using high-fat/high-sucrose diet (HFSD)-fed rats was conducted to investigate the long-term effects of EGCG on systemic metabolism, neuroinflammation, and adipose and skeletal muscle morphology.
RESULTS: Acute oral administration of EGCG or the bitter tastant denatonium benzoate significantly attenuated glycemic excursions and elevated plasma glucagon-like peptide-1 (GLP-1) levels in wild-type mice. Crucially, these effects were completely abolished in Skn-1a-/- mice, identifying bitter taste receptors as essential mediators. In the chronic rat model, repeated oral EGCG treatment effectively reduced food intake, body weight gain, and adiposity. Beyond metabolic regulation, EGCG suppressed Iba-1 expression in the hippocampal dentate gyrus, indicating an anti-neuroinflammatory effect. Notably, EGCG increased the cross-sectional area of both the soleus and extensor digitorum longus muscles across all diet groups, mimicking the beneficial effects of physical exercise.
CONCLUSION: These findings indicate that EGCG acts as a "metabolic trigger" through Skn-1a-dependent chemosensory pathways, primarily involving T2R signaling. By demonstrating that bitter-related chemosensory signaling regulates systemic homeostasis and provides neuroprotective effects, this study supports a new concept of "sensory nutrition." This research positions gastrointestinal and oral chemosensors as a novel and non-invasive therapeutic target for managing metabolic syndrome and cognitive decline, overcoming the limitations of systemic bioavailability.
METHODS: This study utilized wild-type and Skn-1a-/- mice (lacking bitter taste signaling) to evaluate acute metabolic responses. Furthermore, a chronic study using high-fat/high-sucrose diet (HFSD)-fed rats was conducted to investigate the long-term effects of EGCG on systemic metabolism, neuroinflammation, and adipose and skeletal muscle morphology.
RESULTS: Acute oral administration of EGCG or the bitter tastant denatonium benzoate significantly attenuated glycemic excursions and elevated plasma glucagon-like peptide-1 (GLP-1) levels in wild-type mice. Crucially, these effects were completely abolished in Skn-1a-/- mice, identifying bitter taste receptors as essential mediators. In the chronic rat model, repeated oral EGCG treatment effectively reduced food intake, body weight gain, and adiposity. Beyond metabolic regulation, EGCG suppressed Iba-1 expression in the hippocampal dentate gyrus, indicating an anti-neuroinflammatory effect. Notably, EGCG increased the cross-sectional area of both the soleus and extensor digitorum longus muscles across all diet groups, mimicking the beneficial effects of physical exercise.
CONCLUSION: These findings indicate that EGCG acts as a "metabolic trigger" through Skn-1a-dependent chemosensory pathways, primarily involving T2R signaling. By demonstrating that bitter-related chemosensory signaling regulates systemic homeostasis and provides neuroprotective effects, this study supports a new concept of "sensory nutrition." This research positions gastrointestinal and oral chemosensors as a novel and non-invasive therapeutic target for managing metabolic syndrome and cognitive decline, overcoming the limitations of systemic bioavailability.