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Abstract-The risk for an adverse pregnancy outcome is markedly higher in women with history of preeclampsia. This may stem from impaired placentation in early gestation and from high impedance to flow in uteroplacental circulation. The renin-angiotensin system is one of the mediators of the remodeling of spiral arteries throughout pregnancy. The D allele of the Insertion/Deletion (I/D) polymorphism in the ACE gene has been associated with higher ACE activity, accounting for 47% of the total phenotypic variance of serum enzyme levels. To investigate whether the ACE I/D polymorphism affects maternal uteroplacental and fetal umbilical circulation and the pregnancy outcome in women with a history of preeclampsia, 106 women underwent Doppler examination of uterine arteries resistance index and umbilical artery pulsatility index at the 16th, 20th, and 24th weeks of gestation and were genotyped for the I/D polymorphism. This study found a difference in genotype distribution (Pϭ0.0002) and allele frequency (PϽ0.0001) between women with and those without preeclampsia recurrence and fetal growth restriction as well as an association (Pϭ0.0007) between DD genotype and risk of recurrent preeclampsia or fetal growth restriction. At the 16th, 20th, and 24th weeks, uterine artery resistance indexes were significantly lower in II, higher in DD, and intermediate in ID genotype carriers, whereas the umbilical artery pulsatility index values were significantly higher in the DD group in comparison to ID and II genotypes. Key Words: angiotensin-converting enzyme Ⅲ polymorphism Ⅲ preeclampsia Ⅲ pregnancy T he risk for an adverse pregnancy outcome in women who have previously had preeclampsia is markedly higher (from 20% to 40%) 1,2 in comparison to women with history of normal pregnancy, but the mechanisms involved have not yet been identified. The maternal syndrome of preeclampsia (PE) and the fetal syndrome of fetal growth restriction (FGR) during the latter half of pregnancy are believed to result from impaired placentation in early gestation. 3,4 Deficient placentation is characterized by inadequate trophoblast invasion into the maternal spiral arteries and a failure to develop lowresistance uteroplacental circulation. 3 Doppler ultrasonographic studies of uteroplacental 5 and fetal umbilical circulation 6 have shown that high impedance to flow is associated with subsequent PE, FGR, and related complications.Previous experimental studies 7 suggested that the "physiological remodeling" of spiral arteries throughout pregnancy is mediated by the renin-angiotensin system (RAS), which is one of the main factors regulating blood pressure, and fluid and electrolyte balance. 8 Throughout normal pregnancy, the RAS is stimulated; plasma renin activity, angiotensinogen, angiotensin II, and aldosterone levels are all increased. 9 At the same time, pregnancy induces a refractoriness to the pressor effects of angiotensin II. 10 In patients with PE, a significant association between the T235 molecular variant of the angiotensinogen (AGT) gene, ...

OBJECTIVE -To assess the 24-h glucose levels in a group of nondiabetic, nonobese pregnant women and to verify the presence of correlations between maternal glucose levels and sonographic parameters of fetal growth. RESEARCH DESIGN AND METHODS -A total of 66Caucasian nonobese pregnant women with normal glucose challenge tests (GCT) enrolled in the study; from this population, we selected 51 women who delivered term (from 37 to 42 weeks completed) live-born infants without evidence of congenital malformations. The women were requested to have three main meals and to perform daily glucose profiles fortnightly from 28 -38 weeks without modifying their lifestyle or following any dietary restriction. All subjects were taught how to monitor their blood glucose by using a reflectance meter. Fetal biometry was evaluated by ultrasound scan according to standard methodology at 22, 28, 32, and 36 weeks of pregnancy.RESULTS -The overall daily mean glucose level during the third trimester was 74.7 Ϯ 5.2 mg/dl. Daily mean glucose values increased between 28 (71.9 Ϯ 5.7 mg/dl) and 38 (78.3 Ϯ 5.4 mg/dl) weeks of pregnancy. We found a significant positive correlation at 28 weeks between 1-h postprandial glucose values and fetal abdominal circumference (AC). At 32 weeks, we documented positive correlations between fetal AC and maternal blood glucose levels 1 h after breakfast, 1 and 2 h after lunch, and 1 and 2 h after dinner. At 36 weeks, there was a positive correlation between fetal AC and 1-and 2-h postprandial blood glucose levels. In addition, there was a negative correlation between head-abdominal circumference ratio and 1-h postprandial blood glucose values.CONCLUSIONS -This longitudinal study first provides a contribution toward the definition of normoglycemia in nondiabetic, nonobese pregnant women; moreover, it reveals significant correlations of postprandial blood glucose levels with the growth of insulin-sensitive fetal tissues and, in particular, between 1-h postprandial blood glucose values and fetal AC. Diabetes Care 24:1319 -1323, 2001T he complex phenomenon of fetal growth has been thoroughly investigated over past decades (1) but still remains to be fully understood. We know that maternal glucose is one of the most important factors of influence (1,2), and Reece et al. (3) showed that normoglycemia in pregnancy is associated with normal levels of other nutrients, such as amino acids and lipids. For this reason, glycemia is the single maternal metabolic parameter routinely assessed in diabetic pregnancies. Indeed, the criteria for metabolic control and therapeutic strategies of diabetes in pregnancy are based almost exclusively on maternal glucose levels (2). Although there is overwhelming evidence that good perinatal outcomes can be achieved in diabetic pregnancies only with the normalization of maternal glucose values (4 -6), there is no clear definition of normoglycemia in nondiabetic pregnancies. In fact, a very limited number of studies have been performed thus far in the attempt to define maternal glucose l...

Our results suggest that prolonged fetal exposure to hyperglycemia during pregnancy can change neonatal metabolomic profile at birth without affecting the clinical course.