Maternal Glucose Levels Research Articles

Association between maternal glucose and large for gestational outcomes: Real-world evidence to support Hyperglycaemia and Adverse Pregnancy Outcomes (HAPO) study findings.

To compare large for gestational age (LGA) rates by maternal glucose levels in a real-world setting with those in the Hyperglycaemia and Adverse Pregnancy Outcomes (HAPO) study. To examine the association between fasting plasma glucose (FPG), 1- and 2-h on a 75-g oral glucose tolerance tests (OGTT) and LGA. Pregnancies were categorized according to HAPO thresholds. Category-specific LGA rates were compared to those in HAPO. Categories with glucose thresholds below or above the diagnostic criteria for gestational diabetes mellitus (GDM) were labelled as lower and higher/GDM, respectively. GDM pregnancies were further stratified according to FPG or post-load elevations and logistic regression was used to examine their independent association with LGA. In our cohort of 97,032 pregnancies, rates of LGA increased with increasing maternal glucose in lower categories of FPG, 1- and 2-h glucose (trend p<0.01). However, LGA rates in higher/GDM categories were significantly lower in our study than those in HAPO for 1- and 2-h glucose, but not for FPG. Elevated FPG alone was associated with an almost twofold increase in risk of LGA, while elevated post-load glucose alone was associated with a 20% reduction in risk of LGA, compared to negative OGTT. Real-world data confirm the HAPO study findings at lower levels of maternal glycaemia. At higher levels, GDM diagnosis and treatment appear to be effective in reducing rates of LGA in pregnancies with post-load glucose elevations, but not elevated FPG. Elevated FPG is a stronger predictor of LGA than post-load glucose elevations.

Effects of glucokinase activator, DS-7309, on embryo-fetal developmental toxicity in rats and rabbits

The toxicological effects of DS-7309, a glucokinase activator, on pregnancy and embryo-fetal development in rats and rabbits and maternal blood glucose levels were examined. DS-7309 was administered at 3, 10, or 100 mg/kg to rats from Days 7–17 of pregnancy or at 10, 30, or 100 mg/kg to rabbits from Days 6–18 of pregnancy. In rats, maternal hypoglycemia (approximately 50 mg/dL) was seen at 3 and 10 mg/kg, but it recovered 7 h after dosing, leading to no toxic changes. In contrast, continuous severe maternal hypoglycemia (approximately 40 mg/dL, ≥7 h), fetal eye anomalies, and decreased fetal body weight were noted at 100 mg/kg. In rabbits, no fetal anomalies were seen at 10 and 30 mg/kg where maternal blood glucose level dropped to approximately 60–90 mg/dL, but recovered by 7 h after dosing at the latest. In contrast, at 100 mg/kg, severe hypoglycemia (around 60 mg/dL) was maintained and did not recover until 24 h after dosing; it resulted in decreased fetal viability and increased fetal skeleton anomalies. These findings indicate that DS-7309 could lead to embryo-fetal toxicity in rats and rabbits, with such toxicity considered to be related to continuous severe maternal hypoglycemia.

Using Innovative Machine Learning Methods to Screen and Identify Predictors of Congenital Heart Diseases.

Objective: Congenital heart diseases (CHDs) are associated with an extremely heavy global disease burden as the most common category of birth defects. Genetic and environmental factors have been identified as risk factors of CHDs previously. However, high volume clinical indicators have never been considered when predicting CHDs. This study aimed to predict the occurrence of CHDs by considering thousands of variables from self-reported questionnaires and routinely collected clinical laboratory data using machine learning algorithms.Methods: We conducted a birth cohort study at one of the largest cardiac centers in China from 2011 to 2017. All fetuses were screened for CHDs using ultrasound and cases were confirmed by at least two pediatric cardiologists using echocardiogram. A total of 1,127 potential predictors were included to predict CHDs. We used the Explainable Boosting Machine (EBM) for prediction and evaluated the model performance using area under the Receive Operating Characteristics (ROC) curves (AUC). The top predictors were selected according to their contributions and predictive values. Thresholds were calculated for the most significant predictors.Results: Overall, 5,390 mother-child pairs were recruited. Our prediction model achieved an AUC of 76% (69-83%) from out-of-sample predictions. Among the top 35 predictors of CHDs we identified, 34 were from clinical laboratory tests and only one was from the questionnaire (abortion history). Total accuracy, sensitivity, and specificity were 0.65, 0.74, and 0.65, respectively. Maternal serum uric acid (UA), glucose, and coagulation levels were the most consistent and significant predictors of CHDs. According to the thresholds of the predictors identified in our study, which did not reach the current clinical diagnosis criteria, elevated UA (>4.38 mg/dl), shortened activated partial thromboplastin time (<33.33 s), and elevated glucose levels were the most important predictors and were associated with ranges of 1.17-1.54 relative risks of CHDs. We have developed an online predictive tool for CHDs based on our findings that may help screening and prevention of CHDs.Conclusions: Maternal UA, glucose, and coagulation levels were the most consistent and significant predictors of CHDs. Thresholds below the current clinical definition of “abnormal” for these predictors could be used to help develop CHD screening and prevention strategies.

Maternal Glucose and LDL-Cholesterol Levels Are Related to Placental Leptin Gene Methylation, and, Together With Nutritional Factors, Largely Explain a Higher Methylation Level Among Ethnic South Asians.

BackgroundLeptin, mainly secreted by fat cells, plays a core role in the regulation of appetite and body weight, and has been proposed as a mediator of metabolic programming. During pregnancy leptin is also secreted by the placenta, as well as being a key regulatory cytokine for the development, homeostatic regulation and nutrient transport within the placenta. South Asians have a high burden of type 2 diabetes, partly attributed to a “thin-fat-phenotype”.ObjectiveOur aim was to investigate how maternal ethnicity, adiposity and glucose- and lipid/cholesterol levels in pregnancy are related to placental leptin gene (LEP) DNA methylation.MethodsWe performed DNA methylation analyses of 13 placental LEP CpG sites in 40 ethnic Europeans and 40 ethnic South Asians participating in the STORK-Groruddalen cohort.ResultsSouth Asian ethnicity and gestational diabetes (GDM) were associated with higher placental LEP methylation. The largest ethnic difference was found for CpG11 [5.8% (95% CI: 2.4, 9.2), p<0.001], and the strongest associations with GDM was seen for CpG5 [5.2% (1.4, 9.0), p=0.008]. Higher maternal LDL-cholesterol was associated with lower placental LEP methylation, in particular for CpG11 [-3.6% (-5.5, -1.4) per one mmol/L increase in LDL, p<0.001]. After adjustments, including for nutritional factors involved in the one-carbon-metabolism cycle (vitamin D, B12 and folate levels), ethnic differences in placental LEP methylation were strongly attenuated, while associations with glucose and LDL-cholesterol persisted.ConclusionsMaternal glucose and lipid metabolism is related to placental LEP methylation, whilst metabolic and nutritional factors largely explain a higher methylation level among ethnic South Asians.

Developmental Effects of (Pre-)Gestational Diabetes on Offspring: Systematic Screening Using Omics Approaches.

Worldwide, gestational diabetes affects 2–25% of pregnancies. Due to related disturbances of the maternal metabolism during the periconceptional period and pregnancy, children bear an increased risk for future diseases. It is well known that an aberrant intrauterine environment caused by elevated maternal glucose levels is related to elevated risks for increased birth weights and metabolic disorders in later life, such as obesity or type 2 diabetes. The complexity of disturbances induced by maternal diabetes, with multiple underlying mechanisms, makes early diagnosis or prevention a challenging task. Omics technologies allowing holistic quantification of several classes of molecules from biological fluids, cells, or tissues are powerful tools to systematically investigate the effects of maternal diabetes on the offspring in an unbiased manner. Differentially abundant molecules or distinct molecular profiles may serve as diagnostic biomarkers, which may also support the development of preventive and therapeutic strategies. In this review, we summarize key findings from state-of-the-art Omics studies addressing the impact of maternal diabetes on offspring health.

Placental Endocrine Activity: Adaptation and Disruption of Maternal Glucose Metabolism in Pregnancy and the Influence of Fetal Sex.

The placenta is an endocrine fetal organ, which secretes a plethora of steroid- and proteo-hormones, metabolic proteins, growth factors, and cytokines in order to adapt maternal physiology to pregnancy. Central to the growth of the fetus is the supply with nutrients, foremost with glucose. Therefore, during pregnancy, maternal insulin resistance arises, which elevates maternal blood glucose levels, and consequently ensures an adequate glucose supply for the developing fetus. At the same time, maternal β-cell mass and function increase to compensate for the higher insulin demand. These adaptations are also regulated by the endocrine function of the placenta. Excessive insulin resistance or the inability to increase insulin production accordingly disrupts physiological modulation of pregnancy mediated glucose metabolism and may cause maternal gestational diabetes (GDM). A growing body of evidence suggests that this adaptation of maternal glucose metabolism differs between pregnancies carrying a girl vs. pregnancies carrying a boy. Moreover, the risk of developing GDM differs depending on the sex of the fetus. Sex differences in placenta derived hormones and bioactive proteins, which adapt and modulate maternal glucose metabolism, are likely to contribute to this sexual dimorphism. This review provides an overview on the adaptation and maladaptation of maternal glucose metabolism by placenta-derived factors, and highlights sex differences in this regulatory network.

Placental metabolic profiling in gestational diabetes mellitus: An important role of fatty acids.

AimGestational diabetes mellitus (GDM) is the most common metabolic disorder during pregnancy. Accumulating studies have reported metabolites that are significantly associated with the development of GDM. However, studies on the metabolism of placenta, the most important organ of maternal‐fetal energy and material transport, are extremely rare. This study aimed to identify and discuss the relationship between differentially expressed metabolites (DEM) and clinical parameters of the mothers and newborns.MethodsIn this study, metabolites from 63 placenta tissues (32 GDM and 31 normal controls) were assayed by ultra‐performance liquid chromatography‐high resolution mass spectrometry (UPLC‐HRMS).ResultsA total of 1297 annotated metabolites were detected, of which 87 significantly different in GDM placenta. Lipids and lipid‐like molecules accounted for 62.1% of DEM as they were significantly enriched via the “biosynthesis of unsaturated fatty acids” and “fatty acid biosynthesis” pathways. Linoleic acid and α‐linolenic acid appeared to be good biomarkers for the prediction and diagnosis of GDM. In addition, the level of PC(14:0/18:0) was negatively correlated with neonatal weight. 14 metabolites significantly different in male and female offspring, with the most increase in female newborns.ConclusionEven if maternal blood glucose level is well controlled, there are still metabolic abnormalities in GDM. Lipids and lipid‐like molecules were the main differential metabolites, especially unsaturated fatty acids.

Macrosomia and its predictors in pregnant women with diabetes in Ethiopia.

To estimate the prevalence of macrosomia and contributing factors among pregnant women with diabetes in Ethiopia. The Cochrane, PubMed, Google Scholar, SCOPUS, Web of Science electronic databases and grey literature found in online university repositories were searched for primary studies reporting the prevalence of macrosomia (birth weight ≥4kg, irrespective of gestational age) and/or at least one determinant factor using WHO diabetes diagnosis criteria were involved. Variations across the studies were checked using the I2 statistic; funnel plot and Egger's test were used to assess publication bias. A weighted inverse random effect model was used to estimate the overall prevalence of macrosomia. The overall prevalence of macrosomic newborns among pregnant women with diabetes [15.1% (95% CI: 9.0%, 21.2%)] was higher than the prevalence among non-diabetic mothers (3.9%). Maternal blood glucose level >100mg/dl [AOR = 10.5: 95% CI: 5.9, 15.1] and >120mg/dl [AOR = 8.8: 95% CI: 4.5, 13.0], lack of Antenatal Care (ANC) visit [AOR = 10.8: 95% CI: 6.0, 15.0], previous adverse birth outcomes and advanced maternal age [AOR = 3.5: 95% CI: 1.0, 5.9] were significantly associated with the prevalence of macrosomia at 95% CI. The pooled prevalence of macrosomia among pregnant women with diabetes was higher than the prevalence among non-diabetic pregnant women (3.9%). Advanced maternal age, previous adverse birth outcomes, lack of ANC and uncontrolled maternal plasma glucose level were independent predictors of macrosomia.

The effect of phenytoin on embryonic heart rate in Vivo

Phenytoin is a known human teratogen with unknown etiology. Several mechanisms have been proposed including disturbances in folate metabolism, induction of embryonic hypoxia following phenytoin-induced bradycardia, free radical formation following re-oxygenation and phenytoin-induced maternal hyperglycemia.Using high frequency ultrasound, we demonstrated that phenytoin induced a dramatic decrease in the heart rate of embryos. This coincided with a moderate transient decrease in maternal heart rate and blood glucose levels. Embryonic heart rate had not fully recovered 24 h later in some embryos despite normal maternal physiological parameters. In a separate study, extent of hypoxia was measured using the marker pimonidazole. Phenytoin-exposed embryos did not demonstrate increased hypoxia compared to control embryos at 2, 4, 8 or 24 h dosing. Together our results show that phenytoin induces malformations as a result of a combination of insults: embryonic bradycardia, maternal bradycardia and maternal hyperglycemia. However, this does not appear to result in measurable embryonic hypoxia in our animal model.

Association between maternal pregestational glucose level and adverse pregnancy outcomes: a population-based retrospective cohort study

ObjectiveTo investigate the association between maternal pregestational blood glucose level and adverse pregnancy outcomes.DesignRetrospective cohort study.SettingThis study was conducted in the Chongqing Municipality of China between April 2010 and December...

Early Pregnancy Glycemic Levels in Non-Diabetic Women and Pregnancy Outcome: A Retrospective Cross-Sectional Study

BackgroundMaternal fasting blood sugar (FBS) variations within normal range and lower than that in diabetes mellitus (DM) may be associated with adverse feto-maternal outcomes.ObjectiveTo find out if a rise of maternal FBS level above 80 but still below 120 mg/dL (group 2) has an influence on feto-maternal outcomes compared with a maternal FBS below 80 mg/dL (group 1).MethodsRetrospective cross-sectional study. FBS was measured at the booking visit. Subjects whose FBS was measured before 20 weeks were categorized according to their FBS (>80 mg/dL or ≤80 mg/dL) and correlation between FBS levels in the two groups with several parameters were tested.ResultsGroup 1 (130 healthy pregnant women) and group 2 (88 healthy pregnant women) did not show a statistical difference in age or BMI. More statistically significant cases were diagnosed with GDM in group 2 than in group 1 (39.8% vs 16.9%, P value 0.000). More cases that needed pharmacological intervention in the form of metformin or insulin or both were seen in group 2 than in group 1 (p value 0.007 and 0.061, respectively). More but not statistically significant polyhydramnios was seen more in group 2 than in group 1 (9.1% vs 3.1%, p value 0.056). There was no statistically significant difference between the 2 groups in relation to all other fetomaternal outcome parameters that were studied.ConclusionRaised maternal fasting blood glucose level (80–120 mg/dL) in healthy primigravid women in early pregnancy was associated with significant diagnosis of gestational diabetes mellitus and need for pharmacological intervention. An association was found with polyhydramnios but this was not statistically significant. No influence was found on preterm birth, fetal weight, mode of delivery or APGAR score. More attention should be given to FBS levels early in pregnancy to reduce the risk for later complications.

Temporal fluctuations in maternal glucose levels alter placental transcriptome in pregnancies complicated by gestational diabetes

Temporal fluctuations in maternal glucose levels alter placental transcriptome in pregnancies complicated by gestational diabetes

P–597 Placental expression of neurokinin B and its receptor NK3R is increased in women with polycystic ovary syndrome: results of a preliminary study

Abstract Study question Is the placental expression of neurokinin B (NKB) and its receptors NK1R, NK2R and NK3R affected by the polycystic ovary syndrome (PCOS)? Summary answer: The placental expression of NKB and NK3R is increased in PCOS, while the expression of NK1R and NK2R is not affected. What is known already: Women with PCOS are at increased risk of pregnancy complications and poor pregnancy outcomes. Defective placentation is among the proposed mechanisms involved. Altered NKB placental expression has been associated with several conditions characterized by placental dysfunction, such as pre-eclampsia and intra-uterine growth retardation. To our knowledge, the expression of NKB and its receptors has not been studied in placental tissue of women with PCOS. Study design, size, duration This was a single-center, prospective, case-control study. Women with PCOS according to the Rotterdam criteria (cases) and healthy pregnant women (controls) were enrolled at first prenatal visit and followed until delivery. Only women with spontaneous conception and singleton, uncomplicated, term pregnancies (10 PCOS and 10 controls) were included in the final analysis. All participants provided informed consent. Participants/materials, setting, methods At delivery, placental specimens were collected and immediately submerged in RNAlater solution. Samples were stored at –20oC until analysis. The mRNA expression of NKB, NK1R, NK2R and NK3R was quantified by real-time PCR (RT-PCR). The relative mRNA expression was estimated by the ΔΔCT method, using β-actin as reference (housekeeping gene). Statistical analysis was performed using SPSS 25.0, and the level of statistical significance was set at 0.05 (two-sided). Main results and the role of chance The placental mRNA expression of NKB and NK3R was significantly higher in PCOS women versus controls (2.4-fold, p &amp;lt; 0.05 for NKB and 7-fold, p &amp;lt; 0.05 for NK3R). No significant alterations were observed in the mRNA expression of NK1R and NK2R between the two groups. There was no statistically significant difference regarding age, BMI, caesarian section frequency, offspring sex and birth weight between women with PCOS and controls. The placental expression of NKB and its receptors was correlated neither with maternal age and BMI, nor with offspring birth weight. Limitations, reasons for caution The main limitation of this study is the small sample size. Expanding the number of participants is the necessary next step, in order to corroborate our preliminary findings. Furthermore, correlations between the placental expression of NKB, NK1R, NK2R, NK3R and maternal sex steroids, glucose and insulin levels should be sought. Wider implications of the findings: The present study is the first to demonstrate increased placental expression of NKB and its receptor NK3R in women with PCOS. These findings support a potential role for NKB as a mediator of placental alterations characterizing PCOS. Trial registration number Not applicable

Association of maternal vitamin B12 and folate levels in early pregnancy with gestational diabetes: a prospective UK cohort study (PRiDE study)

Aims/hypothesisThe prevalence of gestational diabetes mellitus (GDM) is increasing worldwide in all ethnic groups. Low vitamin B12 and low/high folate levels may contribute to GDM risk, but there is conflicting evidence. Our aim is to assess the relationships of early pregnancy vitamin B12 and folate levels with the risk of GDM status at 26–28 weeks of gestation.MethodsThis was a prospective, multi-centre, multi-ethnic cohort study (n = 4746) in the UK. Participants who were eligible to be selectively screened as per the National Institute for Health and Care Excellence (NICE) criteria were included in the study.ResultsGDM prevalence was 12.5% by NICE and 14.7% by International Association of Diabetes and Pregnancy Study Groups (IADPSG) criteria. Folate deficiency (1.3%) was rare but B12 insufficiency (42.3% at <220 pmol/l) and folate excess (36.5%) were common in early pregnancy. Early pregnancy median B12 levels were lower, and folate levels higher, in women who were diagnosed with GDM at 26–28 weeks. B12 was negatively associated with fasting plasma glucose (1 SD: −0.06 mmol/l; 95% CI −0.04, −0.08; p < 0.0001) and 2 h plasma glucose levels (−0.07 mmol/l; 95% CI −0.02, −0.12; p = 0.004). Higher B12 was associated with 14.4% lower RR of IADPSG-GDM (0.856; 95% CI 0.786, 0.933; p = 0.0004) after adjusting for key confounders (age, parity, smoking status, ethnicity, family history, household income and folate status). Approximately half of this association was mediated through BMI. Folate was positively associated with 2 h plasma glucose levels (0.08 mmol/l; 95% CI 0.04, 0.13; p = 0.0005) but its relationship with fasting plasma glucose was U-shaped (quadratic β: 0.011; p = 0.05). Higher folate was associated with 11% higher RR of IADPSG-GDM (adjusted RR 1.11; 95% CI 1.036, 1.182; p = 0.002) (age, parity, smoking status, ethnicity, family history, household income and B12 status). Although no interactions were observed for B12 and folate (as continuous variables) with glucose levels and GDM risk, a low B12–high folate combination was associated with higher blood glucose level and risk of IADPSG-GDM (adjusted RR 1.742; 95% CI 1.226, 2.437; p = 0.003).Conclusions/interpretationB12 insufficiency and folate excess were common in early pregnancy. Low B12 and high folate levels in early pregnancy were associated with small but statistically significant changes in maternal blood glucose level and higher RR of GDM. Our findings warrant additional studies on the role of unmetabolised folic acid in glucose metabolism and investigating the effect of optimising early pregnancy or pre-conception B12 and folate levels on subsequent hyperglycaemia.Trial registration:ClinicalTrials.gov NCT03008824.Graphical abstract

Associations of maternal insulin resistance during pregnancy and offspring inflammation at birth and at 5 years of age: A prospective study in the Gen3G cohort

BackgroundMaternal insulin resistance is associated with greater maternal inflammation during pregnancy, but its relation to inflammation in offspring remains unclear. The goal of this study was to assess the relationship of gestational insulin resistance and other glycemic markers with offspring inflammation at birth and at 5 years of age. MethodsWe included 653 mother–child pairs from the prospective pre-birth Gen3G cohort. We examined maternal insulin and glucose levels measured during the second trimester of pregnancy, from which we derived the homeostatic model of assessment of insulin resistance (HOMA-IR) and the Matsuda index. We assessed offspring inflammation at birth and at 5 years of age by measuring plasma tumor necrosis factor-α (TNFα) concentrations. We conducted multivariable regression models to evaluate associations of each insulin and glucose marker with offspring inflammation adjusting for confounding variables. ResultsHigher levels of fasting insulin were associated with lower TNFα levels at birth (−0.78, 95% CI [−1.45, −0.11]), in the fully adjusted model. We observed similar associations with the HOMA-IR and opposite direction with the Matsuda index. We did not find persistence of the association between maternal fasting insulin and offspring TNFα at 5 years of age. ConclusionsGreater maternal insulin resistance during pregnancy was associated with lower cord blood TNFα levels in newborns. The mechanisms by which maternal insulin resistance may promote lower inflammatory levels in newborns are not fully understood and more research is needed to deepen our understanding of these mechanisms.

Identification of maternal continuous glucose monitoring metrics related to newborn birth weight in pregnant women with gestational diabetes.

To identify the specific glucose metrics derived from maternal continuous glucose monitoring (CGM) data, which were associated with a higher percentile of offspring birth weight. In this cohort study, we recruited singleton pregnant women with GDM who underwent CGM for 5-14 days at a mean of 28.8 gestational weeks between Jan 2017 and Nov 2018. Commonly used single summary glucose metrics of glucose exposure (including mean 24-h, daytime, and nighttime glucose level) and variability (including J-index and mean amplitude of glycaemic excursions) were derived from CGM data. A novel comprehensive glucose metric-hours per-day spent in a severe variability glucose mode (HSSV)-was identified using the spectral clustering method, which reflects both glucose level and variability. Multiple linear regression models were used to estimate the associations of sex- and gestational age-adjusted birth weight percentile with CGM parameters. Ninety-seven women comprising 127,279 glucose measurements were included. Each 1-SD increase in maternal nighttime mean glucose level and HSSV was associated with 6.0 (95% CI 0.4, 11.5) and 6.3 (95% CI 0.4, 12.2) percentage points increase in birth weight percentile, respectively. No associations were found between other glucose metrics and birth weight percentile. Nighttime mean glucose level has a comparable effect size to HSSV in association with fetal growth, suggesting that endogenous hyperglycemia might drive the association between maternal hyperglycemia and birth weight. Further studies need to examine the effect of lowering nighttime glucose level and/or HSSV on preventing fetal overgrowth in GDM women.

Prediction of insulin treatment in women with gestational diabetes mellitus

IntroductionThe identification of pregnant women with Gestational Diabetes Mellitus (GDM) who will require insulin therapy, may modify their management to closer monitoring and probable early interventions. The aim of the study was to develop a predictive model for the necessity of insulin treatment in women with GDM.Materials and methodsThis was a prospective cohort study. Data from 775 women diagnosed with GDM per the IADPSG criteria were analyzed using logistic regression and a machine learning algorithm, the Classification and Regression Trees (CART). Potential predictors routinely recorded at follow-up visits were tested and used for the development of the model. The resultant model was externally validated using the data from two different perinatology clinics.ResultsPreconceptional maternal BMI and morning fasting blood glucose levels at baseline and at 1 h during an Oral Glucose Tolerance Test (OGTT) were independent significant predictors for the treatment modality of GDM. Baseline blood glucose greater than 98 mg/dl and preconceptional maternal Body Mass Index (BMI) between 26 and 31 kg/height2 increased substantially the probability of insulin therapy (odds ratio [OR] 4.04, 95% confidence interval [CI] CI 2.65–6.17 and 2.21, 95%CI 1.42–3.43, respectively). The area under the curve (AUC) for the internal and external validation of the predictive model was 0.74 and 0.77, respectively.ConclusionsA simple model based on maternal characteristics and the values of an OGTT can predict the need for insulin treatment with accuracy. Overweight women with an abnormal baseline blood glucose at OGTT are at high likelihood for insulin treatment.Key messageFifteen to 30% of women with Gestational Diabetes Mellitus (GDM) require insulin therapy. Overweight women with baseline blood glucose greater than 98 mg/dl at OGTT are at increased risk for insulin treatment and close monitoring and increased physical exercise are required.

Maternal Glycemia During Pregnancy and Early Offspring Development: A Prospective Birth Cohort Study.

The association of maternal gestational diabetes mellitus (GDM) with neurodevelopmental outcomes remains controversial and evidence that maternal increasing levels of glucose during pregnancy associated with the risk for impaired neurodevelopment were limited. To identify the continuous association of increasing maternal glucose levels with neurodevelopmental disorders in offspring and explore the potential contribution of cord metabolites to this association. The prospective birth cohort study included 1036 mother-child pairs. Primary predictors were maternal exposure GDM and maternal glucose values at a 75-g oral-glucose-tolerance test at 24 to 28 weeks during pregnancy. Primary neurodevelopmental outcomes at 12 months in offspring were assessed by the Ages and Stages Questionnaires, Third Edition (ASQ-3). Maternal GDM was associated with failing the communication domain in offspring in the adjusted models [relative risk (RR) with 95% CI: 1.97 (1.11, 3.52)]. Increasing levels of fasting plasma glucose (FPG), 1-h plasma glucose (1-h PG) and 2-h plasma glucose (2-h PG) with 1 SD change were at higher risks in failing the personal social domain of ASQ-3 [RRs with 95% CI for FPG: 1.49 (1.09, 2.04); for 1-h PG: 1.70 (1.27, 2.29); for 2-h PG: 1.36 (1.01, 1.84)]. The linear association was also demonstrated. Compared with girls, boys exposed to higher maternal glucose levels were inclined to the failure of the personal social domain. Mediation analysis showed the contribution of maternal GDM to failure of communication domain mediated by C-peptide. Maternal glucose levels below those diagnostic of diabetes are continuously associated with impaired neurodevelopment in offspring at 12 months.

155 Evening blue light exposure, maternal glucose and infant birth weight

Abstract Introduction During pregnancy, the use of light-emitting electronic devices before bedtime may contribute to or exacerbate sleep problems. Exposure to blue-wavelength light in particular from these devices may affect sleep by inhibiting melatonin release and causing neurophysiologic arousal which may affect the uterus environment. However, the health consequences of blue-wavelength light on maternal glucose level and fetus development is poorly understood. The purpose of this study was to test the hypothesis that nocturnal blue-light exposure is associated with maternal glucose level and infant’s birth weight. Methods A group of pregnant women aged 24-39 years old who wore 7-day actigraphy, and completed questionnaires including Pittsburgh Sleep Quality Index participated in the study. Infant’s birth weight (n=41) and fasting glucose level (n=30) was abstracted from mothers’ medical charts. Blue-wavelength light exposure was obtained from actigraphy recordings. Unadjusted linear regression analyses were performed to determine sleep characteristics that were associated with fasting glucose and infant’s weight (p&amp;lt;0.2). Using infant’s birth weight and fasting glucose as outcome variables, confounding variables were evaluated in full linear regression models as independent variables. Results The mean gestational age was 30.66 (Standard Deviation (SD) 3.46) weeks. The mean fasting glucose, infant’s birth weight and gestational age at delivery were 95.73 mg/dL (SD 24.68), 3261 gr (SD 470) and 38.78 (SD 1.69), respectively. In unadjusted analysis, infant birth weight was significantly associated with only blue light value (μW/cm2) (β=76.98, p=0.002) and remained significant (β=78.26, p=0.003) after adjusting for BMI, maternal age and gestational diabetes. Fasting glucose was associated with blue light value (β=2.81, p=0.055) and became significantly associated (β=78.26, p=0.003) after adjusting for sleep duration, parity and gestational diabetes. The coefficient demonstrates that for each unit increase in the evening blue light exposure, there is a 78 gr increase in infant weight after controlling the effect of maternal age, BMI and gestational diabetes. Conclusion Evening blue light exposure during mid and late pregnancy may alter maternal glucose regulation and placental nutrient transport to fetus, but these remain to be studied. This study may shed light on future research on the effect of evening light exposure on pregnancy outcomes. Support (if any) National Institutes of Health (R00-NR013187)

2020 NICE guideline update: Good news for pregnant women with type 1 diabetes and past or current gestational diabetes.

In December 2020, the National Institute for Health and Care Excellence (NICE) reviewed the evidence and updated their recommendations on intermittently scanned (commonly known as Flash) and Continuous Glucose Monitoring (CGM) during pregnancy for women with type 1 diabetes (1). The NICE guidelines now recommend offering CGM to all pregnant women with type 1 diabetes to help them meet their pregnancy glucose targets and improve neonatal outcomes. Their evidence review, based on the CONCEPTT randomised trial (2) and a Swedish observational study (3) found that, compared to capillary glucose monitoring, CGM resulted in more women achieving their blood glucose targets, fewer caesarean sections and fewer neonatal intensive care admissions.