Introduction: We have previously shown that fetuses of mothers with gestational diabetes mellitus (GDM) and insulin resistance exhibit a prolongation of fetal auditory evoked brain responses (fAER) compared to fetuses of normal glucose tolerant (NGT) women during an oral glucose tolerance test (OGTT). This implies that maternal metabolism may program the fetal brain. We asked whether a positive family history of type 2 diabetes (FHD) without metabolic programing also impacts fetal brain activity. We therefore investigated brain activity in fetuses of NGT mothers with positive FHD.
Methods: A 75g OGTT was administered to healthy pregnant women. Glucose and insulin levels were measured after 0, 60 and 120 minutes. Each blood extraction was preceded by magnetoencephalographic recordings of fAER. From a group of 151 participants, a sub-sample of 53 women, 38 with a negative and 15 with a positive FHD (at least one first- or second-degree relative) was selected based on the following inclusion criteria: no GDM, BMI 18.5-30 kg/m², no preterm birth, no change in fetal position, at least two fMEG with detectable fetal responses.
Results: There were no significant differences in age, BMI at delivery, weight gain during pregnancy and gestational age between the groups. Maternal glucose levels and insulin sensitivity determined by glucose and insulin measurements during the OGTT were not significantly different. Manova with gestational age as covariate showed a significant interaction between measurement timepoint and FHD on fAER latency (F(2)=4.96, p=0.009). Fetuses of mothers with positive FHD had a prolonged fAER (273±109ms) compared to fetuses of mothers with negative FHD (218±67ms) at 60 minutes during the OGTT (F(1)=5.21, p=0.027).
Discussion: In addition to the previously shown influence of maternal metabolism on fetal brain activity, a positive maternal FHD also appears to delay fetal brain activity. This can be due to the genetic or environmental influence which is linked to a positive FHD.
F. Schleger: None. L. Walter: None. M. Heni: Research Support; Self; Boehringer Ingelheim GmbH. Speaker's Bureau; Self; Boehringer Ingelheim GmbH, Merck Sharp & Dohme Corp., Novo Nordisk Inc.. S.Y. Brucker: None. H. Haering: None. A. Fritsche: Advisory Panel; Self; Sanofi-Aventis Deutschland GmbH, Novo Nordisk A/S, Eli Lilly and Company, Boehringer Ingelheim GmbH. H. Preissl: None.
