DNA methylation is a conservative epigenetic marker. A correct DNA methylation pattern is essential for embryonic development. Mammalian embryos gain a complete de novo DNA methylation design around implantation. DNA methylation is a potential mechanism of periconceptional programming, suggesting that the DNA methylation pattern of developing embryo might be affected in distinct ways, depending on nutritional and hormonal signals. To expand this idea we have investigated the DNA methylation pattern of the promoter region of the POU5F1 (Oct4) pluripotency gene in preimplantation rabbit embryos at day 6 p.c (early gastrulation stage). The blastocysts were collected from healthy and diabetic rabbits. The POU5F1 promoter contains four conservative regions, which are embracing important elements for its transcription: proximal and distal enhancers (PE-1A, PE-1B, DE-1A), a SOX2/Oct4 binding site and hormone responding element (HRE). We have characterized the CpG islands methylation at all mentioned regions in two embryonic tissues: embryoblast and trophoblast, using bisulfite treatment, cloning and sequencing. The analysis has been successfully performed for the trophoblast tissue yet. A higher methylation of the CpG islands for HRE and at the beginning of first exon has been noticed in the trophoblast of diabetic embryos. A hypomethylation in trophoblast from diabetic embryos comparing to trophoblasts from healthy pregnancies was visible for proximal enhancer 1A (PE-1A) in frame of conservative region 3 (CR3). In this context, DNA methylation can be considered as a form of embryo developmental plasticity, which can promote metabolic disorders in adult life.