The incidence of diabetes mellitus for young people rises since years. A preconceptional diabetes mellitus leads to subfertility. Most of the causes for a diabetic subfertility are still unknown. Stress can significantly deteriorate glycemic control in diabetes. Several mechanisms by which "stress hormones", like adrenaline and cortisol or corticosterone, can contribute to the regulation of glucose homeostasis have been identified. Using reverse transcription-polymerase chain reaction (RT-PCR) and quantitative real-time RT-PCR, we examined the expression of adrenergic receptors and the glucocorticoid receptor transcripts in the female rabbit reproductive tract and in gastrulating blastocysts developed in normoinsulinemic mothers and in mothers with experimentally induced diabetes mellitus type 1. The glucocorticoid receptor expression was detected in the reproductive tract as well as in gastrulating blastocysts at a high level. In maternal endometrium, α1D-, α2A-, β1-, and β2-adrenergic receptors were expressed, whereby β1 transcript was not detectable in the endometrium from diabetic mothers. In preimplantation embryos, all 9 adrenergic receptors were expressed, most of them predominantly in the embryoblast. A maternal diabetes mellitus altered α2A-adrenergic receptor expression in the blastocyst and reversed the ratio of α2A transcript quantity between embryoblast and trophoblast. Our results show that the maternal reproductive tract and the preimplantation embryo express a distinct pattern of the stress response system. Alterations in the pattern and/or in functionality are likely linked to subfertility in diabetes mellitus.
Keywords: adrenergic receptors; diabetes mellitus; early pregnancy; gastrulating blastocyst; glucocorticoid receptor; reproductive tract.