Additionally, we attempted to dissect the mechanisms by which EGCG mitigated β-cell disturbances, and found that EGCG inhibited experimental diabetes triggered by a high-sucrose-high-fat (HSHF) diet and streptozotocin (STZ) administration by increasing upregulating pancreatic PDX-1 and MafA. The gene discussed is PDX1; the disease is diabetes mellitus.