Diabetes during pregnancy is associated with aortic remodelling in the fetus, stimulating the development of cardiovascular diseases in adult life. However, studies suggest that the use of foods high in omega-3 fatty acid, such as flaxseed oil, may reverse this effect of metabolic programming. This study aimed at investigating whether the effects of diabetes in mothers are passed on to their offspring in a gender-specific manner and whether the flaxseed oil used during pregnancy and lactation reverses or not the possible negative effects of this programming. Diabetic female rats (n = 18) were mated and allocated into three groups (n = 6): high-fat group (HG); flaxseed oil group (FOG) and control group (CG) (nondiabetic rats) during pregnancy and lactation. On the 21st day, male and female pups were weaned on a standard diet until 180 days. Aorta histomorphometry was analysed. Intima-media layer thickness was larger in FOG than CG in male (+15%) and than HG in female (+13.7%). Male FOG (+11.5%) showed higher amount of elastic fibre than CG. Maternal intake of flaxseed oil during pregnancy and lactation of diabetic mothers program the offspring to increase aorta intima-media layer thickness in adulthood and preserves aorta elastic fibres deposition in male offspring.

We extracted L., the newborn of a diabetic mother, for antenatal diagnostic of myocardial hypertrophy and anomaly of foetal heart rate. Post-natal echocardiography showed severe septal myocardial hypertrophy with latero-basal myocardial akinesia. We did not observe a Doppler gradient through the left ventricular outflow. Selective coronary angiography showed an occlusion of the circumflex artery. Myocardial hypertrophy is a classic complication in newborns of diabetic mothers. The mother’s diabetes and neonatal infarction remain an exceptional association. We discuss a different hypothesis to explain coronary occlusion and how myocardial infarction avoided septal obstruction.

We describe a newborn who had echocardiogaphic features of severe hypertrophic cardiomyopathy and duct-dependent systemic blood flow. Blood flow to the upper body could be maintained only by prostaglandin El, as in the case of hypoplastic left heart syndrome. Forward flow was gradually established from the left ventricle, and the patient weaned from prostaglandin El. Although the patient's mother had poorly controlled diabetes, the patient at 24 months of age shows residual but lessened ventricular hypertrophy and increased cavity size.

Several factors have been found recently to have a significant impact on newborn bone mineral content (BMC) and developing fetal bone. Recently we showed that maternal vitamin D deficiency may affect fetal bone mineralization. Korean winter-born newborn infants had extremely low serum 25-hydroxyvitamin D (25-OHD), high serum cross-linked carboxy-terminal telopeptide of type I collagen (ICTP; a bone resorption marker), and markedly lower (8 %) total body BMC than summer-born newborn infants. Infant total body BMC was positively correlated with cord serum 25-OHD and inversely correlated with ICTP, which was also negatively correlated with vitamin D status. In three separate studies on North American neonates we found markedly lower (8–12 %) BMC in summer newborn infants compared with winter newborn infants, the opposite of the findings for Korean neonates. The major reason for the conflicting BMC results might be the markedly different maternal vitamin D status of the North American and Korean subjects. Recently, we found evidence of decreased bone formation rates in infants who were small-for-gestational age (SGA) compared with infants who were appropriate-for-gestational age; we reported reduced BMC, cord serum osteocalcin (a marker of bone formation) and 1,25-dihydroxyvitamin D (the active metabolite of vitamin D), but no alterations in indices of fetal bone collagen metabolism. In theory, reduced utero-placental blood flow in SGA infants may result in reduced transplacental mineral supply and reduced fetal bone formation. Infants of diabetic mothers (IDM) have low BMC at birth, and infant BMC correlated inversely with poor control of diabetes in the mother, specifically first trimester maternal mean capillary blood glucose concentration, implying that factors early in pregnancy might have an effect on fetal BMC. The low BMC in IDM may be related to the decreased transplacental mineral transfer. Cord serum ICTP concentrations were higher in IDM than in control subjects, implying increased intrauterine bone resorption. BMC is consistently increased with increasing body weight and length in infants. Race and gender differences in BMC appear in early life, but not at birth. Ethanol consumption and smoking by the mother during pregnancy affect fetal skeletal development.