OC 03.05: Gestational diabetes, endothelial damage and metabolomics markers

Abstract

INTRODUCTION: Gestational diabetes (GDM) can determine modifications of metabolic fetal pathways, programming the progeny to development possible future cardiovascular and metabolic disorders. This fetal endothelial dysfunction may be detectable by measuring the aorta intima media thickness (aIMT). Metabolomics performs an integrated assessment of the variance in levels in metabolites connetted to a pathological condition. METHODS: This was an exploratory multidisciplinary study. Patients referred to tertiary center for morphological scan were selected and then divided according to those who later developed GDM or not. Inclusion criteria were singleton pregnancies, a correct dating of pregnancy and diagnosis of gestational diabetes (HAPO 2011). Fetal biometry, fetal well being, maternal and fetal abdominal aortic intima media thickness (aIMT), fetal aorta diameter and fetal aorta pulsatility index were measured at 35 weeks of gestation. At delivery a sample of cord blood for a metabolomic evaluation was collected. Statistical analysis Mann-Whitney (p<0.05) was used. RESULTS: 35 patient were included, 20 with GDM and 15 controls. Patients with GDM are older and nulliparous than controls. At 35 weeks the fetal aIMT was significantly increased in cases compared to controls (0.72 vs. 0.52 mm, p = 0.002), as well as the fetal aortic diameter, with a positive correlation between aortic PI and fetal aIMT in the GDM group. Maternal GDM aIMT was significantly higher with a positive correlation with fetal GDM aIMT (p 0.05). No significant differences exist in relation to body mass index gestational age at delivery, birth weight, mode of delivery and Apgar score. In case group metabolomic analysis showed an higher expression of Fenilalanina, Leucina, Isoleucina, Alanina and Triptofano than control one. CONCLUSIONS: Newborns of mothers with gestational diabetes have an increased intima-media thickness and aortic abdominal PI. The metabolomic identification of different expression of amino acids involved in the glucose homeostasis in cases, together with the presence of a subclinical vascular modification, may subtend a fetal adaptation to impaired glucose tolerance.