Epidemiologic studies have clearly identified modifications of fetal environment as a risk factor for the development of cardiovascular diseases in adulthood.

In our experimental model, rats exposed in utero to maternal diabetes develop an hypertension as early as 6-month of age. In order to determine if the development of this hypertension results from an abnormal vascular fetal programming, gene expression profile of the aorta was studied on oligonucleotides chips (Agilent, G4130, 22k). Arterial structure and elastic properties were assessed on 3-(non-hypertensive stage) to 18-month-old rats from control (CMO3 and CMO18) and diabetic mothers (DMO3 and DMO18), with echo-tracking device and histomorphometry. DMO had a significantly higher SBP than CMO at 6 and 18 months of age (DMO18 : 218±3 mmHg vs CMO18 : 155±2 mmHg). DMO3 are characterized by an over-expression of subunits of P450 (Cyp4f4, Cyp4f2, Cyp8b1) and an under-expression of prostacyclin receptor, which both could contribute to vasoconstriction. Carotid elastic properties were not significantly different between CMO and DMO at 3 and 6 months. Surprisingly, thoracic aorta of DMO was not significantly thicker than CMO at 6 and 18M, in spite of the higher level of SBP in DMO. The lack of BP-induced wall thickening in DMO3 can be related to the under-expression of genes coding for proteins involved in migration and cell-matrix interaction (Evl, Ckap4, Dcamkl1). In conclusion, these results suggest an abnormal vascular fetal programming in rats exposed in utero to maternal hyperglycemia, which could explain the structural and functional arterial disorders observed in this model.