Growth hormone and fertility in oMt1a-oGH transgenic mice

Female mice carrying a regulatable growth hormone transgene (oMt1a-oGH) are subfertile when the transgene is actively expressed. This study was design ed to characterize subfertility caused by increased concentrations of growt h hormone. In particular, this study aimed to: (i) determine the effects of transgene activation and inactivation on mating, conception, maintenance o f pregnancy, ovulation rate, litter characteristics and embryonic survival at day 17 of pregnancy, (ii) characterize oestrous cyclicity in transgenic versus wild-type female mice, and (iii) correlate corticosterone concentrat ions with transgene expression and reproductive performance. Transgenic and wild-type female mice were allocated randomly to one of four treatment gro ups at weaning: (i) transgenic female mice that always express the transgen e, (ii) transgenic female mice that never express the transgene, (iii) tran sgenic female mice that express the transgene for up to 8 weeks of age and (iv) non-transgenic wild-type female mice receiving the transgene stimulus until 8 weeks of age. Activation followed by inactivation of the transgene resulted in an increased incidence of remating, resulting in an extended in terval to establish pregnancy in comparison with all other treatment groups . Transgenic mice that always expressed the transgene and those that expres sed the transgene for up to 8 weeks of age had lower pregnancy rates and hi gher ovulation rates compared with mice from other treatment groups. Both e mbryonic survival and the duration of the oestrous cycle did not differ amo ng treatment groups. Active expression of the transgene resulted in an incr ease in the plasma concentration of corticosterone, which was associated wi th reduced fertility. These data indicate that the presence of a high growt h hormone concentration impedes the establishment and maintenance of pregna ncy. Increased plasma corticosterone concentrations may interfere with impl antation as well as potentiate leptin resistance, which has been reported p reviously in studies with these mice.