Kisspeptin neuropeptides stimulate release of GnRH to initiate puberty and maintain mammalian fertility. Kisspeptins are encoded by the Kiss1 gene and directly stimulate GnRH neurons via the G-protein coupled receptor, GPR54. Transgenic mice with inactivating mutations of Kiss1 or Gpr54 are sterile and have hypogonadotrophic hypogonadism caused by a failure to secrete GnRH. The aim of this study was to determine whether the sterility of mutant female mice was solely caused by absence of central kisspeptin signalling or whether there are additional defects in the ovaries. To study this, we used a hormone replacement protocol to mature the reproductive axis of Kiss1 and Gpr54 mutant mice. The mutant mice were bred with fertile males and evaluated for maintenance of pregnancy. Although, the mutant mice were induced to ovulate, none of the mice maintained pregnancy past E6.5 of gestation. It was found that the mutant mice had significantly lower levels of progesterone compared to wild-type pregnant mice. Ovary transplantation studies showed that mutant ovaries implanted into wild-type mice could support pregnancy to term indicating that there was no intrinsic defect in the mutant ovaries. Progesterone replacement allowed pregnancy to progress normally past E6.5. We hypothesise that the failure of the mutant mice to maintain progesterone levels during pregnancy is caused by inadequate luteotrophic stimulation of the corpus luteum due to central kisspeptin signalling defects.