Pre-gestational type 1-diabetes (T1D) increases the risk of miscarriage and congenital malformations and programs the offspring to develop metabolic syndrome at adulthood. Management of maternal diabetes is essential during the gestation but could be also highly important around the conception. Using a rabbit model, the effects of maternal T1D during the periconceptional period on preimplantation blastocysts has been well documented 3'5, but the effects on feto-placental phenotype at 28dpc (term=31 days) need to be explored. Diabetes was induced by Alloxan in dams 7 days before mating. Glycemia was maintained at 15-20mmoi/L with exogenous insulin injections. At 4dpc, embryos were collected and transferred into non­ diabetic recipients. At 28 dpc, control (C) and diabetic (D) fetuses were collected for biometric records, placental analyses including stereology and gene expression and lipid profiles of feto-placental tissues by gas chromatography. Lipid data were analyzed by principal component analysis. D-fetuses were growth retarded, hyperglycemic and dyslipidemic compared to C. Moreover, Placental efficiency was much higher in D than in C-fetuses. The volume density of fetal vessels was significantly decreased in D-placentas compared to C-placentas, whereas the volume density of trophoblast tended to increase (p=0.051). This morphometric disruption was associated to a deregulation of the expression of genes related ta nutrient supply and lipid metabolism. ln fetal plasma, a specific fatty acid signature was observed in D and C-groups. Moreover, the composition of placenta! and letal liver membranes differed according to maternal status and fetal sex. Tissues from D-fetuses contained significantly more omega-6 polyunsaturated fatty acids compared to C. Docosahexaenoic acid decreased while linoleic acid increased in the cardiac membranes of D-fetuses, indicating a higher risk of ischemia. This study demonstrates that an exposure ta high plasma glucose during the short periconceptional period is sufficient to adversely program fetal phenotype by reducing fetal growth, altering placental function and lipid profiles in all fetal tissues.