Effects of gestational diabetes on fetal oxygen and glucose levels in vivo

Abstract

Objective Fetal hypoxia and acidemia have been reported in pregestational diabetic pregnancies in relation to poor glycaemic control, but it is still uncertain whether this is the case in apparently well-controlled gestational diabetes.Population and methods Maternal arterial and umbilical venous and arterial blood samples were collected from 37 normal (N) and 38 pregnancies complicated by gestational diabetes (GDM) at the time of caesarean section.Main outcome measures Respiratory gases, acid-base balance, lactate and glucose concentrations were measured.Results Both fetal and placental weights were significantly increased in GDM compared to N pregnancies, despite similar gestational age. Maternal biochemical parameters were similar in N and GDM but GDM fetuses were significantly more hypoxic (O 2 saturation: N 63.2 ± 13.9; GDM 53.8 ± 14.6%, P < 0.01; O 2 content: N 5.5 ± 1.4; GDM 4.8 ± 1.2 mmol/l, P < 0.05). Glucose (N 3.4 ± 0.5, GDM 3.9 ± 1.2 mmol/l, P < 0.05) and lactate (N 1.32 ± 0.49; GDM 1.64 ± 0.75 mmol/l, P < 0.05) concentrations were significantly increased in the umbilical vein in GDM compared to N fetuses. Placental histology was consistent with altered villous morphology.Conclusions Our data indicate that fetuses from gestational diabetic mothers have increased umbilical glucose concentrations despite normal maternal glucose levels and a reduction in oxygen saturation and O 2 content together with increased lactate concentration, reflecting altered fetal metabolism. These data suggest that 'good maternal metabolic control' achieved by currently used methods of monitoring glucose control is not sufficient to ensure a normal oxygenation status and metabolic milieu for the fetus in GDM pregnancies.

Umbilical Cord Blood Acidosis in Term Pregnancies With Gestational Diabetes Mellitus and Its Relations to Maternal Factors and Neonatal Outcomes

“…UCB acidosis was significantly more detected among these neonates, compared to term neonates who were born to healthy mothers; these results are consistent with other studies (8,15). In the study of Taricco et al, although reduction in oxygen saturation and O 2 content combined with increased lactate concentration were observed in the fetuses of GDM mothers, the rate of UCB acidosis and UCB pH were not different between the GDM and non-GDM mothers (14). This could be due to the tight control of glucose levels and GDM during the 3rd trimester in the study of Taricco et al, while in our study many women did not have good glucose control.…”

“…All the participants had undergone a routine glycemic screening for GDM at 28 -32 gestational weeks with a non-fasting oral GCT, in which venous blood was sampled 1 hour after a 50-g oral glucose load. If the 1-hour glucose result was ≥ 140 mg/dL, the participant was referred for a 100-g fasting glucose 3-hour GTT (14). Based on the ACOG (16), normal GTT results were a blood glucose level < 95 mg/dL at baseline, < 180 mg/dL at 1 hour, < 155 mg/dL at 2 hours, and < 140 mg/dL at 3 hours.…”

“…UCB acidosis is not always suggestive of acute neonatal stress, rather it can happen in chronic conditions with placental dysfunction including gestational diabetes mellitus (GDM) and preeclampsia (8)(9)(10), in which impairment of placental blood flow can affect trans-placental gas exchange, placing the fetus at risk for chronic hypoxia and acidosis (11)(12)(13). The high rate of chronic fetal acidosis, placental insufficiency in chronic conditions like preeclampsia and GDM (10,14,15), and fetal adaptation to these conditions through changes in fetal circulation might affect the value of UC-ABG analysis in the prediction of adverse neonatal outcomes in these special populations (10); previously, we showed that UCB acidosis might not be a good Copyright © 2018, Iranian Red Crescent Medical Journal. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/) which permits copy and redistribute the material just in noncommercial usages, provided the original work is properly cited predictive of adverse neonatal outcomes in pregnancies with preeclampsia, probably due to fetal adaptation to chronic acidosis and placental dysfunction (10).…”

Amniotic Fluid Oxidative and Nitrosative Stress Biomarkers Correlate with Fetal Chronic Hypoxia in Diabetic Pregnancies

“…However, perinatal mortality and morbidity in type 1 diabetic pregnancies has remained practically unchanged in the last two decades [2,3]. Fetal plasma and amniotic fluid (AF) erythropoietin (EPO) levels are frequently elevated in diabetic pregnancies suggesting an increased incidence of chronic fetal hypoxia, especially in patients with poor glycemic control [4,5,6]. Although the pathogenesis of chronic fetal hypoxia in diabetic pregnancies is not fully understood, several maternal, placental and fetal factors have been implicated [7].…”

Midtrimester amniyotik sıvı leptin ve insülin düzeyleri ile gestasyonel diabetes mellitus ilişkisi

“…Ayrıca ketogenezde değişim ve beta hidrosibutirat konsantrasyonunda artışa neden olur. Sonuçta glukoneogenez artar, ürik asit artar ve hipoksiye sebep olabilir [3][4][5][6][7]. İnsülin pankreasta beta hücrelerden salgılanan bir hormondur ve kandan glukozun hücreye alınmasını sağlar.…”