Obesity is an escalating global epidemic caused by an imbalance between energy intake and expenditure. (−)-Epigallocatechin-3-gallate (EGCG), the major polyphenol in green tea, has been reported to be conducive to preventing obesity and alleviating obesity-related chronic diseases. However, the role of EGCG in energy metabolism disorders and central nervous system dysfunction induced by a high-fat diet (HFD) remains to be elucidated. The aim of this study was to evaluate the effects of EGCG on brown adipose tissue (BAT) thermogenesis and neuroinflammation in HFD-induced obese C57BL/6J mice. Mice were randomly divided into four groups with different diets: normal chow diet (NCD), normal chow diet supplemented with 1% EGCG (NCD + EGCG), high-fat diet (HFD), and high-fat diet supplemented with 1% EGCG (HFD + EGCG). Investigations based on a four-week experiment were carried out including the BAT activity, energy consumption, mRNA expression of major inflammatory cytokines in the hypothalamus, nuclear factor-kappa B (NF-κB) and signal transducer and activator of transcription 3 (STAT3) phosphorylation, and immunofluorescence staining of microglial marker Iba1 in hypothalamic arcuate nucleus (ARC). Experimental results demonstrated that dietary supplementation of EGCG significantly inhibited HFD-induced obesity by enhancing BAT thermogenesis, and attenuated the hypothalamic inflammation and microglia overactivation by regulating the NF-κB and STAT3 signaling pathways.

Obesity is closely associated with neuroinflammation in the hypothalamus, which is characterized by over-activated microglia and excessive production of pro-inflammatory cytokines. The present study was aimed at elucidating the effects of (−)-epigallocatechin gallate (EGCG) on palmitic acid-stimulated BV-2 microglia and high-fat-diet-induced obese mice. The results indicated the suppressive effect of EGCG on lipid accumulation, pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) release, and microglial activation in both cellular and high-fat-diet rodent models. These results were associated with lower phosphorylated levels of the janus kinase 2/signal transducers and activators of transcription 3 (JAK2/STAT3) signaling pathway. In conclusion, EGCG can attenuate high-fat-induced hypothalamic inflammation via inhibiting the JAK2/STAT3 signaling pathways in microglia.

Lately, matcha green tea has gained popularity as a beverage and food additive. It has proved to be effective in preventing obesity and related metabolic syndromes. However, the underlying mechanisms of its control effects against non-alcoholic fatty liver disease (NAFLD) are complicated and remain elusive. In the present study, we performed an in vivo experiment using male C57BL/6 mice fed with a high-fat diet and simultaneously treated with matcha for six weeks. Serum biochemical parameters, histological changes, lipid accumulation, inflammatory cytokines, and relevant indicators were examined. Dietary supplementation of matcha effectively prevented excessive accumulation of visceral and hepatic lipid, elevated blood glucose, dyslipidemia, abnormal liver function, and steatosis hepatitis. RNA sequencing analyses of differentially expressed genes in liver samples indicated that matcha treatment decreased the activity of lipid droplet-associated proteins and increased the activity of cytochrome P450 enzymes, suggesting improved metabolic capacity and liver function. The current study provided evidence for new dietary strategies based on matcha supplementation to ameliorate lipotoxicity-induced obesity and NALFD.

Dietary components significantly impact human health, influencing diverse physiological processes from metabolic homeostasis to cognitive function and aging. Tea, a widely consumed functional beverage rich in antioxidants, has gained attention for its health benefits. Epigallocatechin gallate (EGCG), the most abundant and bioactive catechin in green tea, is renowned for its potent biological activities. However, the direct absorption of EGCG is limited due to its low oral bioavailability, with a substantial portion reaching the colon where it interacts extensively with gut microbiota. This microbial interplay is crucial for EGCG's biotransformation and the realization of its health-promoting potential, yet the underlying mechanisms remain to be fully elucidated. This review synthesizes EGCG's structural features, metabolism, and interactions with gut microbiota, summarizing its roles in gut health and systemic effects through gut-related axes, and outlines future research. First, it elaborates EGCG's structural features, as a flavan-3-ol with a polyphenolic structure containing multiple hydroxyl groups, whose antioxidant and bioactive properties are associated with the specific arrangement of benzene rings and the gallate moiety. Second, it outlines its metabolic process, limited absorption in the small intestine, enzymatic metabolism in the small intestine and liver (including methylation, glucuronidation, and sulfation), and extensive biotransformation in the colon by gut microbiota into metabolites such as epigallocatechin and gallic acid. Third, it explores its effects on the gut, modulating gut microbiota composition by promoting beneficial bacteria and inhibiting pathogenic strains, enhancing intestinal barrier function by upregulating tight junction proteins, and promoting the production of short-chain fatty acids. Finally, it elucidates how EGCG modulates key gut-related health pathways and its broader implications for systemic health through various interconnected gut axes, including the gut-liver, gut-brain, gut-renal, and gut-lung axes, and concludes by outlining prospective research directions aimed at further elucidating the potential of EGCG in promoting health.