Sensory receptor study: Green tea elevates glucose tolerance and GLP-1 through taste receptors

Researchers in Japan and Italy observed improvements in glucose metabolism and muscle size, as well as neuroprotective effects, in animals administered a green tea supplement, with effects mediated by sensory receptors. “By demonstrating that bitter-related chemosensory signaling regulates systemic homeostasis and provides neuroprotective effects, this study supports a new concept of ‘sensory nutrition,” they wrote in Frontiers in 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.” Bitter compounds in plant foods have known health benefits, but the mechanisms underlying their effects in the body are still not fully understood. Previous research shows that taste receptors for bitter compounds (T2Rs) are present in tissues outside the mouth, including the brain, heart, reproductive system, and respiratory system, suggesting a role beyond taste perception. Evidence suggests that enteroendocrine cells in the gut may secrete hormones in response to bitter compounds and regulate glucose and energy balance. While bitter compounds in green teas, such as epicatechin and epigallocatechin, can regulate blood glucose, they are poorly absorbed in the body. This “bioavailability paradox” prompted researchers to hypothesize that the biological activities are mediated by sensory receptors rather than through systemic circulation. The current study administered epigallocatechin gallate (EGCG), the primary green tea flavanol, in wild-type mice and mice lacking bitter taste signaling to assess their acute metabolic responses. An additional study investigated the long-term effects of EGCG in rats fed a high-fat/high-sucrose diet (HFSD) for six weeks. The researchers found that the EGCG significantly improved glucose tolerance and elevated glucagon-like peptide-1 (GLP-1) levels, but only in the wild-type mice. The lack of these effects in the knockout mice suggested that bitter taste receptor signaling is essential for EGCG’s primary metabolic effects. “These findings suggest that T2Rs function as essential sensors that trigger metabolic responses immediately upon oral or gastric exposure, independent of systemic absorption,” the researchers wrote. The findings in the chronic model indicated that EGCG treatment “effectively reduced food intake, body weight gain, and adiposity.” Additionally, the supplement exhibited anti-inflammatory effects and increased muscle area, “mimicking the beneficial effects of physical exercise”. The researchers proposed that the effects in skeletal muscle and the brain are driven by the sensory characteristics of EGCG, specifically its astringency, which is distinct from its bitterness. Sensory neurons detecting the astringency may enhance the sympathetic nervous system via the sympathetic-adrenal medullary (SAM) axis, they noted. This, in turn, releases noradrenaline and adrenaline, which can help to burn fat and synthesize muscle. “EGCG and similar astringent compounds represent promising candidates for next-generation functional foods designed to prevent obesity-related cognitive decline and sarcopenia,” the researchers concluded. Acknowledging the limitations of animal studies, the researchers noted that human trials are necessary to confirm if the sensory nutrition pathways are similar. Source: Frontiers in Nutrition , https://doi.org/10.3389/fnut.2026.1863138 , “Sensory signaling mediates the systemic metabolic and neurological effects of epigallocatechin gallate.” Authors: Y. Yoshida et al.