Resistin (Rstn) is known as an adipocyte-specific secretory hormone that can cause insulin resistance and decrease adipocyte differentiation. In contrast, green tea catechins, especially (-)-epigallocatechin gallate (EGCG), have been reported as a body weight and diabetes chemopreventative. Whether EGCG regulates production of Rstn is unknown. Using 3T3-L1 adipocytes, we found that EGCG at 20 and 100 µM suppressed Rstn mRNA levels by about 35% and 50%, respectively, after 3 h. The basal half-life of Rstn mRNA induced by actinomycin D was more than 12 h, but it shifted to 3 h in the presence of EGCG. This suggests that EGCG regulates the stability of Rstn mRNA. Treatment with cycloheximide did not prevent EGCG-suppressed Rstn mRNA levels, suggesting that the effect of EGCG does not require new protein synthesis. Intracellular Rstn protein significantly decreased in the presence of 100 µM EGCG 3 h after treatment while the release of the Rstn protein did not significantly change. This suggests that EGCG may modulate the distribution of Rstn protein between the intracellular and extracellular compartment. EGCG did not affect amounts of Erk1/2, phospho-JNK, phospho-p38, and phospho-Akt proteins, but reduced amounts of phospho-Erk1/2 proteins. Overexpression with MEK1 blocked EGCG-inhibited Rstn mRNA expression. These data suggest that EGCG downregulates Rstn expression via a pathway by which is dependent on the Erk pathway.