Type-1 diabetes (T1D) is caused by the reduction in pancreatic insulin secretion, inducing chronic hyperglycemia. Pre-gestational 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 highly important around the conception. The aim of this study was to explore the effects of maternal TD1 during the periconceptional period on feto -placental phenotype at 28dpc (term=31days), according to the sex of the conceptus. Diabetes was induced by Alloxan in dams 7 days before mating. Glycemia was maintained at 15-20mmol/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 and lipid analysis of feto -placental tissues by gas chromatography. Data were analyzed by principal component analyses. D-fetuses were growth retarded, hyperglycemic and dyslipidemic compared to C. A specific fatty acid signature was observed in fetal plasma. The composition of placental and fetal liver membranes differed according to maternal status and fetal sex. Tissues from Dfetuses contained significantly more omega-6 polyunsaturated fatty acids compared to C. No biochemical signature was observed in the immature fetal heart, but docosahexaenoic acid was decreased and linoleic acid increased in the cardiac membranes of D-fetuses, indicating a higher risk of ischemia. This study demonstrates that an exposure to high plasma glucose during the short periconceptional period reduces fetal growth and alters the lipid profiles in all fetal tissues.