The present study investigates the mechanism by which obesity associated rise in leptin and insulin levels cause anovulation in vespertilionid bat, Scotophilus heathii. In the ovary of S. heathii, leptin and insulin receptors were mainly localized in interstitial and thecal cells and in the granulosa cells of primary follicles suggesting its possible role in androgen synthesis and follicular development. Adiposity associated increase in circulating leptin level down regulate ovarian LH-receptor expression and produce characteristic morphological changes in the antral follicles, such as hypertrophy of granulosa cells and a sharp decline in the rate of proliferation as well as apoptosis in the antral follicles. These follicles are referred as unique antral follicle. The in vitro study confirmed the in vivo findings that the high dose of leptin suppresses apoptosis and LH receptors. The present study thus showed that the adiposity associated increase in leptin during the first phase of follicular development inhibits folliculogenesis and simultaneously suppresses both follicular proliferation and apoptosis by reducing sensitivity to gonadotropin stimulation and decreasing circulating LH levels.