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Epigallocatechin-3-gallate (EGCG) is beneficial for inhibiting dyslipidemia and reducing hyperlipidemic risk. The purpose of the present study was to investigate the glycolipid regulatory effects and potential mechanisms of EGCG in a high‑fat diet and streptozotocin‑induced type 2 diabetes mellitus (T2DM) mouse model. The results demonstrated that EGCG can decrease blood glucose levels and increase insulin resistance in T2DM mice. In addition, EGCG can regulate serum lipid levels, including those of total cholesterol, triglyceride and low‑density lipoprotein receptor (LDL‑r), and reduce lipid deposition in vascular endothelial cells in a dose‑dependent manner. In addition, the gene and protein expression of related scavenger receptors, including cluster of differentiation 36, sterol regulatory element binding protein 2 (SREBP), SREBP cleavage‑activating protein and LDL‑r, were downregulated in a dose‑dependent manner. The present study noted that EGCG possesses potential as a natural product for preventing and treating metabolic hyperlipidemia syndrome, probably by reducing the blood lipid levels, alleviating vascular endothelial cell damage, maintaining normal lipid metabolism in blood vessels and ameliorating glycolipid disorders.

Anti‑glycolipid disorder effect of epigallocatechin‑3‑gallate on high‑fat diet and STZ‑induced T2DM in mice