Leptin (LEP) is implicated in the pathogenesis of polycystic ovary syndrome (PCOS). This study investigates the mechanism of LEP in PCOS. The baseline information of 80 PCOS patients and matched controls was analyzed, with serum and follicular fluid (FF) LEP and LEP receptor (LEPR) levels, telomerase activity, and relative telomere length (TL) measured. The correlation of FF LEP with telomerase activity and TL was analyzed. The viability and apoptosis of KGN cells (the ovarian granulosa cells) treated with gradient LEP were assessed. LEP-LEPR interaction was examined. LEPR, v-myc avian myelocytomatosis viral oncogene homolog (c-MYC), and telomerase reverse transcriptase (TERT) levels and c-MYC protein expression in the TERT promoter region were determined. Nuclear c-MYC translocation was detected. LEP was upregulated in sera and FF of PCOS patients. FF LEP positively correlated with telomerase activity and TL. Low-concentration LEP facilitated KGN cell proliferation, and high-concentration LEP dose-dependently suppressed cell proliferation, promoted apoptosis, upregulated LEPR, and increased telomerase activity and relative TL. LEP-LEPR interaction upregulated c-MYC and facilitated its nuclear accumulation. c-MYC enrichment in the TERT promoter region upregulated TERT, altering telomerase activity and TL and inducing cell apoptosis. Briefly, LEP/LEPR activates c-MYC, modulates TERT expression, and increases telomerase activity and TL, thus inducing ovarian granulosa cell apoptosis and participating in PCOS.