Justification: Intrauterine exposure to type 1 or type 2 diabetes increase the risk of macrosomia (35 % to 50 % versus 10 % in general population) despite a good glycemic control. The consequences are : shoulder's dystocia, lung immaturity, caesarean section, neonatal hypoglycaemia and a high frequency of obesity and metabolic disorders in adults. The mechanisms of macrosomia are unclear; chronic hyperglycemia and subsequent hyperinsulinaemia observed during the diabetic pregnancy might explain only partially the fetal weight. Considerable interest has been generated over the last decade on the lipids and fatty acids alterations in diabetes pregnancies. Change in lipoproteins metabolism have been described associated with macrosomia. Maternal nutrition before and during pregnancy plays an important role in fetal growth and subsequent development of an increased susceptibility to obesity and diabetes in later life. Main objective: Looking for an association between maternal and fetal blood lipid parameters and birth weight and body fat in a context of type 1 or type 2 diabetes. Secondary objectives: * Identify lipid markers associated with fetal macrosomia. * Analyze the placenta by measuring the expression of genes implicated in the storage and the transfer of fatty acids. * Analyze and compare the expression level of placental genes subjected to parental imprinting and validated in animal models.
See this in plain English?
AI-rewrites the medical criteria so a patient or caregiver can understand them. Always confirm with the trial site.
fetal weight corrected by gestational age
Timeframe: just after delivery