Metformin is a drug frequently used during pregnancy in the treatment of type 2 diabetes and disorders associated with insulin resistance. Most studies have focused efforts towards the effects of metformin on neural function and locomotion after birth, with few studies having investigated the consequences of in utero exposure to metformin during embryo or fetal development. Consequently a paucity of data exists aimed at understanding the effects of metformin on the reproductive function of offspring. The aim of the present study was to assess the effects of maternal metformin administration during pregnancy on the fertility of male offspring. Sperm quality analysis and immunohistochemistry were performed to measure these effects. A significant reduction of about 25% was observed in litter size from those males exposed to metformin in utero when compared to control males. We found no differences in testis size at puberty (25dpp: days post-partum) or at the adult stage (90dpp). This is contrary to our previous results which showed a decrease in fetal and neonatal testis size following in utero metformin exposure, and suggests a gradual return to normal growth after birth for the testes. Compared with controls, metformin exposed males had a reduction in seminiferous tubule diameter (141±1µm and 133±1µm, respectively;P<0.05), and germ cell number per seminiferous tubule (65±2 and 57±2, respectively;P<0.05) at 25dpp. There was a significant increase in the number of sperm head abnormalities from males exposed to metformin in utero. However, there were no differences in sperm mobility between groups. Moreover, intratesticular testosterone concentration remained unchanged, whereas in utero exposed males had lower LH concentrations in the pituitary. Exposed adult males presented with significantly more visceral adipose tissue. In conclusion we have shown that embryo/fetal metformin exposure has consequences on the fertility of male offspring, principally by affecting the quality of sperm.