Epigallocatechin gallate and lipid metabolism: intestinal fate, metabolite clusters, and regulatory mechanisms.

Epigallocatechin gallate (EGCG), a principal bioactive constituent of tea, exhibits substantial activity in regulating lipid metabolism. Although EGCG has been extensively studied, an integrated synthesis of its actions across lipid metabolic pathways remains lacking. This review summarizes the intestinal metabolic fate of EGCG and delineates its regulatory mechanisms in fatty acids (FAs), triglycerides, and cholesterol metabolism. By integrating evidence from multiple perspectives, we provide a mechanistic rationale and assess the translational potential of EGCG-based nutritional interventions for diseases associated with lipid dysregulation. EGCG is enzymatically metabolised in the small intestine and liver, and the colonic microbiota then transforms it into lower-molecular-weight, more readily absorbable metabolites, including phenyl-γ-valerolactones (PVLs) and phenolic acids. These metabolites may act in concert with EGCG to modulate key lipid metabolic axes. Specifically, EGCG coordinates AMPK-mediated control of de novo lipogenesis and fatty acid oxidation, induces lipid droplet-targeted lipophagy to reduce intracellular triglyceride burden, and interacts with phosphatidylcholine to disrupt cholesterol's mixed-micelle solubilization, thereby inhibiting intestinal cholesterol absorption. The combined impact of EGCG and its derived metabolites across these pathways suggests a coordinated mechanistic network underlying its effects on lipid metabolism. Finally, we highlight that EGCG's system-level effects are strongly shaped by microbiota-derived metabolites, which may act as key effectors across organs and targets. We conclude by outlining priorities for future research.