Male foetal sex is recognised as an independent risk factor for adverse pregnancy outcomes including preterm birth, neonatal care unit admission and lower Apgar scores. Male foetuses appear to increase the risk of maternal gestational diabetes in the mother due to impacts on beta cell function, and in pregnancies impacted by gestational diabetes, male offspring have higher rates of hypoglycaemia, respiratory distress and macrosomia. Metformin exposure in animal models has also demonstrated sex-specific effects with different patterns in adiposity and lipid levels observed between male and female offspring exposed to metformin in utero. The aim of this analysis is to determine whether foetal sex modifies maternal and neonatal outcomes in gestational diabetes, and evaluate the sex-specific response to metformin on insulin usage, fasting glucose at 32 and 38 weeks and foetal size. We conducted a secondary analysis of the Early Metformin in Gestational Diabetes (EMERGE) randomised controlled trial and analysed neonatal outcomes according to sex and metformin exposure. At randomisation, women carrying a male foetus had a higher plasma glucose at 60 min on oral glucose tolerance testing (9.69 vs. 9.37 mmol/L, p = 0.039). In exploratory analyses, metformin exposure in male pregnancies was associated with lower fasting glucose at 32 (4.88 vs. 5.01 mmol/L, p = 0.014) and 38 weeks (4.49 vs. 4.69 mmol/L, p = 0.002) and reduced insulin use (38% vs. 53%, p = 0.014), with smaller effects in female pregnancies. Metformin-exposed females had higher rates of birth weight < 2500 g compared to those exposed to placebo (8.3% vs. 1.9%, p = 0.032), which was not observed in metformin-exposed males. More male offspring had a birth weight > 4000 g compared to female offspring regardless of metformin exposure. However, the sex-by-treatment interaction was not significant, so these findings should be regarded as hypothesis-generating. Glucometer data suggested a greater mean glucose reduction in males than females (0.29 mmol/L (95% CI 0.29-0.30) versus 0.21 mmol/L (95% CI 0.20-0.21)). Further follow-up is required to determine whether foetal sex influences long-term effects of metformin in pregnancy.

Craniofacial microsomia (CFM), a congenital anomaly stemming from first and second branchial arch dysplasia, poses challenges due to its diverse clinical manifestations, necessitating a comprehensive understanding of its complex etiology. We explored gene-environment interactions in CFM, focusing on genetic factors, and environmental influences, aiming to enhance insights into its multifactorial origins and guide future research. Genetic studies suggest HOXA2, PAX3, and TBX1 as potential susceptibility genes, while epidemiological research links maternal smoking, diabetes, and alcohol use to increased risk. Gene-environment interactions may impact craniofacial development via epigenetic mechanisms, though the exact pathways remain unclear. Future studies should expand CFM cohorts for better G×E risk assessment and apply multiomics approaches to clarify mechanisms. Functional validation via animal models and stem cells will verify genetic and environmental impacts. Advancing personalized medicine with early screening, precise diagnostics, and prevention remains crucial for high-risk cases.

To investigate whether maternal diabetes in pregnancy was associated with altered neonatal global IgG repertoire and early-life infections in offspring. This study included 2,702 mother-infant pairs enrolled at birth and followed longitudinally at the Boston Medical Center. Maternal diabetes and infant infections were extracted from electronic medical records. Cord blood IgG antibodies against a wide range of microbes were quantified using Phage ImmunoPrecipitation Sequencing. Overall, 327 infants (12.1%) were born to mothers with gestational diabetes mellitus (GDM) and 138 (5.1%) to mothers with pregestational diabetes mellitus (PDM). Of these, 416 infants (15.4%) and 1,425 infants (52.7%) had at least one infection in the neonatal period and the first 6 months of life, respectively. Compared with no diabetes, both maternal GDM (risk ratio [RR] 1.20, 95% CI 1.09-1.32) and PDM (RR 1.28, 95% CI 1.12-1.47) were significantly associated with an elevated risk of infections in infants during the first 6 months. These associations were particularly pronounced among infants born preterm, delivered via cesarean section, or with lower IgG repertoire diversity. Additionally, PDM was associated with a lower newborn's global IgG repertoire diversity, compared with no diabetes, with the effect more marked among infants whose mothers had prepregnancy overweight or obesity. This study provides strong evidence of an increased infection risk in the infants of mothers with diabetes and a reduced IgG repertoire diversity in those of PDM mothers. Lower IgG diversity exacerbated the diabetes-infection link. These findings suggest that maternal metabolic conditions may impact an infant's passive immunity and susceptibility to infections.

Evaluating the effects of maternal diabetes on early infant neurodevelopment with a novel combination of four neurodevelopmental tools.

Exposure to Type 1 and Type 2 Maternal Diabetes is Associated with Stage 3-5 Retinopathy of Prematurity

The impact of maternal chronic hypertension in pregnancy on offspring long-term respiratory morbidity.

To quantify the extent to which rising rates of severe maternal morbidity (SMM) in the United States from 2016 to 2022 are attributable to increasing prevalence of maternal risk factors, including advanced maternal age, obesity, pregestational diabetes mellitus, gestational diabetes, chronic hypertension, and hypertensive disorders of pregnancy (HDP). We conducted a retrospective cohort study using the Nationwide Readmissions Database from 2016 to 2022, representing more than 25 million weighted delivery hospitalizations. The primary outcome of SMM was identified with the Centers for Disease Control and Prevention's 21-condition algorithm; a secondary outcome excluded transfusion to improve specificity. Temporal trends in SMM and maternal risk factors were assessed with the Cochran-Armitage test. To quantify the contribution of changes in risk factor prevalence to the overall increase in SMM, we applied a parametric g-computation-based decomposition comparing standardized risks in 2016 and 2022, including counterfactual scenarios in which the distribution of each risk factor was held at 2016 levels. Between 2016 and 2022, the prevalence of SMM increased from 1.5% to 2.2%, and nontransfusion SMM rose from 0.7% to 1.0% (both P<.001). The prevalence of HDP rose from 9.8% to 16.6%, chronic hypertension from 1.4% to 2.6%, and obesity from 9.7% to 15.4%. All maternal risk factors were independently associated with higher odds of SMM. Decomposition analysis showed that HDP accounted for 32.4% (95% CI, 31.2-33.7%) of the increase in SMM and 51.3% (95% CI, 48.5-54.9%) of the increase in nontransfusion SMM. Chronic hypertension and obesity also contributed meaningfully, whereas advanced maternal age and gestational diabetes accounted for a smaller share of the increase. The rise in SMM in the United States is partially attributable to the growing burden of chronic hypertension, HDP, and obesity. These findings highlight the urgent need for preventive interventions targeting cardiometabolic health before, during, and after pregnancy.

BackgroundTransient isolated right ventricular hypertrophy (RVH) is an infrequently recognized cause of early neonatal cyanosis and prolonged oxygen requirement, closely mimicking cyanotic congenital heart disease or persistent pulmonary hypertension of the newborn.MethodsWe present a narrative review of published neonatal cases of transient isolated RVH and describe illustrative observations from four term neonates managed at a tertiary neonatal unit over a 3-year period. Clinical features, antenatal exposures, echocardiographic findings, management, and outcomes were reviewed. A focused literature search identified previously reported neonatal cases.ResultsIncluding the present cohort, 18 neonatal cases have been described to date. Most neonates presented within the first day of life with cyanosis. Echocardiography demonstrated isolated RVH with preserved biventricular function and absence of structural heart disease; premature ductal closure was documented in several cases. Identified risk factors included fetal or perinatal distress, maternal exposure to nonsteroidal anti-inflammatory drugs or corticosteroids, maternal diabetes, and polyphenol-rich substances. Clinical improvement occurred with supportive care, and follow-up echocardiography showed regression of RVH within 4-12 weeks.ConclusionsTransient isolated RVH represents a benign, self-limiting cause of early neonatal cyanosis. Awareness of this phenotype and its natural history may help avoid unnecessary investigations/interventions.

This retrospective case series presents the characteristic features of superior segmental optic nerve hypoplasia (SSONH) in four patients who were initially misdiagnosed with normal-tension glaucoma (NTG), aiming to raise awareness of this rare condition in Türkiye. Four patients (two females and two males) with a mean age of 38 years were included. All were initially diagnosed with NTG and treated with brimonidine drops for three years. Comprehensive ophthalmological examinations were performed, including optic disc photography, optical coherence tomography retinal nerve fiber layer (RNFL) analysis, and visual field testing, with follow-up evaluations conducted over at least one year. Bilateral involvement was observed in two cases, and unilateral involvement in the other two. History of maternal diabetes was noted in 50% of the patients. During medication-free follow-up, all patients demonstrated stable structural and functional parameters, supporting the diagnosis of SSONH. These findings suggest that SSONH should be considered in young patients presenting with superior RNFL thinning and corresponding inferior visual field defects. The non-progressive nature of the condition helps differentiate it from glaucomatous optic neuropathy. Recognizing unilateral cases is essential for avoiding misdiagnosis.

This study aimed to investigate the association between advanced maternal age (AMA) and the risk of gestational diabetes mellitus (GDM) and to evaluate the potential mediating roles of maternal body mass index (BMI) and fetal fraction (FF) measured in non-invasive prenatal testing (NIPT). A retrospective cohort study was conducted among 2,163 singleton pregnancies that underwent NIPT at 13-22weeks' gestation, were diagnosed with GDM at 24-28weeks' gestation, and delivered at a tertiary care hospital in China. Participants were categorized into the AMA group (≥ 35years, n = 575) and non-AMA group (< 35years, n = 1588). Logistic and linear regression models were used to assess the association between AMA and BMI at NIPT, FF, and GDM risk, adjusting for confounders. Mediation analysis was performed to quantify the proportion of the total effect of AMA on GDM mediated by BMI and FF. Compared with the non-AMA group, the AMA group had significantly higher rates of GDM (36.52% vs. 19.65%, P < 0.001), higher BMI (23.30 ± 3.07 vs. 22.51 ± 3.21kg/m2, P < 0.001), and lower FF (10.43% ± 3.65% vs. 11.17% ± 4.14%, P < 0.001). AMA (adjusted OR = 2.49, 95% CI 1.96-3.16, P < 0.001) and higher BMI (adjusted OR = 1.12 per kg/m2, 95% CI 1.08-1.15, P < 0.001) were independently associated with increased GDM risk, while lower FF (per 1% decrease) was also significantly associated with a higher GDM risk (adjusted OR = 1.06, 95% CI 1.03-1.09, P < 0.001). AMA was also associated with both higher BMI (adjusted β = 0.57, 95% CI 0.24-0.90, P < 0.001) and lower FF (adjusted β = -0.58, 95% CI -0.99 to -0.16, P = 0.007). Mediation analysis indicated that BMI and FF mediated 7.08% and 4.36% of the total effect of AMA on GDM risk, respectively (both P < 0.001). AMA significantly increases GDM risk, partly mediated by elevated BMI and reduced NIPT-derived FF. These findings highlight the role of maternal metabolic and placental factors as key intermediaries in AMA-related GDM, offering insights for targeted prenatal risk stratification and intervention. Given the retrospective design, causal inference cannot be established.

Approximately half of the epilepsy cases lack a documented cause. Despite growing evidence linking maternal diabetes to pregnancy complications and impaired child neurodevelopment, little is known about its potential association with child epilepsy. This study aims to determine whether intrauterine exposure to maternal pre-existing type 1 diabetes mellitus (T1DM), type 2 diabetes mellitus (T2DM), or gestational diabetes mellitus (GDM) increases the risk of epilepsy in children. This study included live-born children without major malformations in Sweden from 1998 to 2021. Children were followed from birth until epilepsy diagnosis, death, emigration, or October 2023. Child epilepsy, maternal T1DM, T2DM, GDM, and a comprehensive set of covariates were identified through linked national health registers. Multivariable Cox proportional hazards regression was used to examine the association between maternal diabetes and child epilepsy, estimating adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs). Analyses also included paternal T1DM and T2DM as negative control exposures to assess potential genetic confounding. Preeclampsia, preterm birth, and birth asphyxia were evaluated as mediators, using a sequential mediation approach. Of the 2,305,051 children, 14,283 (0.6%) were exposed to maternal T1DM, 3,833 (0.2%) to T2DM, and 36,388 (1.6%) to GDM. Over a median follow-up of 13years (range 0 to 25.8years), 18,968 were diagnosed with epilepsy, corresponding to an incidence rate of 63.7 per 100,000 person-years. Compared with no maternal diabetes, maternal T1DM and T2DM were associated with increased hazards of epilepsy in children, with aHRs of 1.30 (95% CI 1.11-1.52) and 1.41 (95% CI 1.01-1.97), respectively. Preterm birth and birth asphyxia jointly mediated nearly half of the total effect of T1DM (HRIndirect Effect:1.14, 95% CI: 1.11, 1.17) and 30% of the total effect of T2DM (HRIndirect Effect:1.11, 95% CI: 1.04, 1.18). Paternal T1DM and T2DM, as well as maternal GDM, were not associated with epilepsy risk. In this large cohort study, maternal T1DM and T2DM were associated with an increased risk of epilepsy in children. These associations are likely influenced by intrauterine mechanisms and were partially mediated by preterm birth and asphyxia-related conditions at birth.

Background: Mesenchymal stem cells (MSCs) exhibit a high capacity for differentiation, possess anti-inflammatory and proangiogenic properties, and stimulate the growth and proliferation of neighboring cells. MSCs are a promising tool in regenerative medicine. However, the molecular mechanisms underlying the properties of these cells are not yet fully understood. Gene expression in MSCs influences their characteristics and differentiation potential. Therefore, it is essential to investigate factors affecting gene expression as well as those activating signaling pathways, which will enable more effective and individualized applications of MSCs. In this study, we aimed to identify signaling pathways involved in gene expression in umbilical cord-derived MSCs (UC-MSCs) that may be altered by maternal diabetes and hypothyroidism during pregnancy. Methods: The research material consisted of UC-MSCs. Samples obtained from nine participants were analyzed. UC-MSCs were isolated and cultured, and RNA was extracted. The isolated RNA was used for microarray-based gene expression analysis. Subsequently, pathway enrichment analysis was performed to identify the signaling pathways involved. Results: In the diabetes group, 340 genes (0.71%) were upregulated, while 268 genes (0.56%) were downregulated compared with UC-MSCs from the control group. In the diabetes group, the most compact module was composed of proteins associated with WNT/planar cell polarity (WNT/PCP) signaling. The second module included genes related to smooth muscle activity. In the hypothyroidism group, an association was identified between the extracellular matrix organization pathways (GO:0030198) and the extracellular structure organization (GO:0043062) pathways. Moreover, in this group, increased expression of MMP1, MMP10, and GREM1 was observed. Conclusions: In summary, our study demonstrated the impact of diabetes and hypothyroidism on gene expression in UC-MSCs. We also observed the activation of distinct signaling pathways depending on the presence of these conditions. However, this work represents a preliminary screening, and the results should be validated by PCR in a larger cohort.

Maternal diabetes increases offspring risk for neurodevelopmental disorders, but its association with delayed developmental milestones is unknown. We examined milestone attainment in offspring of mothers with gestational diabetes mellitus (GDM) and pregestational type 1 and type 2 diabetes compared with unexposed controls. We examined a nationwide retrospective cohort study of 466,462 term singleton infants born January 2018 to December 2021 using linked national maternal-child health clinic and hospital discharge data. Developmental data were obtained from nurse-administered structured assessments at routine well-child visits through 24 months of age. Adjusted hazard ratios (aHRs) and 95% CIs for failure to attain developmental milestones were estimated by diabetes type and infant sex. Pregestational diabetes was associated with increased risk for delayed milestone attainment in language, personal-social, and gross motor domains compared with control groups. Offspring of mothers with type 1 diabetes showed the highest risk, followed by those with type 2 diabetes. The association between type 1 diabetes and developmental delay was primarily driven by female offspring, with elevated risks in personal-social (aHR, 1.64; 95% CI, 1.14-2.36), language (aHR, 1.44; 95% CI, 1.09-1.89), and gross motor (aHR, 1.41; 95% CI, 1.05-1.89) domains. GDM was associated with modestly increased risk limited to the fine motor domain (aHR, 1.11; 95% CI, 1.06-1.16). Pregestational diabetes is associated with delayed milestone attainment, with risk varying by diabetes type, developmental domain, and infant sex. Further research should explore long-term trajectories to inform early intervention for children exposed to maternal diabetes.

We sought to evaluate the association between the timing of new-onset hypertensive disorders of pregnancy (HDP) development (ie, antepartum, intrapartum, or postpartum) and the risk of incident hypertension 2-7 years after delivery in nuMoM2b (Nulliparous Pregnancy Outcomes Study: Monitoring Mothers-to-Be) and nuMoM2b-HHS (the nuMoM2b Heart Health Study). This is a secondary analysis of a multisite prospective observational cohort study conducted at eight clinical sites that enrolled nulliparous individuals with singleton pregnancies in their first trimester who were followed during pregnancy and subsequently underwent a cardiovascular screening visit 2-7 years after delivery. For this analysis, we excluded individuals with prepregnancy chronic hypertension in their nuMoM2b pregnancy. We compared rates of stage 1 hypertension (blood pressure 130/80 mm Hg or higher or use of antihypertensive medications) at the 2-7 year postpartum study visit based on the timing of the onset of HDP (categorized as antepartum, intrapartum, postpartum) with no HDP (referent). Multivariable logistic regression models adjusted for baseline covariates (age, insurance, tobacco use, diabetes, and early pregnancy body mass index [BMI]) were used to generate adjusted odds ratios (aOR) and 95% CIs. Interaction analysis was performed to evaluate effect modification by the presence of severe features of HDP. P<.05 was considered statistically significant. Of 4,342 individuals included in this analysis (mean age 27.0 years [SD 5.6 years]), 23.2%% (n=1,007) had new-onset HDP. Among those with HDP, 53.6% (n=540) were diagnosed antepartum, 42.4% (n=427) were diagnosed intrapartum, and 4.0% (n=40) were diagnosed postpartum. At a mean follow-up of 3.2±0.9 years after delivery, the frequency of incident hypertension was elevated regardless of whether HDP occurred antepartum (37.6%, n=203), intrapartum (26.0%, n=111), or postpartum (40.0%, n=16) (compared with no HDP [16.5%, n=550]). After adjustment for maternal age, insurance type, tobacco use, prepregnancy diabetes, and early pregnancy BMI, the risk of chronic hypertension remained elevated regardless of when HDP was diagnosed, although the risk was higher when it developed antepartum (aOR 2.40, 95% CI, 1.95-2.95) or postpartum (aOR 2.90, 95% CI, 1.49-5.64) compared with when it developed intrapartum (aOR 1.55, 95% CI, 1.21-1.97; referent no HDP, P<.01 for all). New-onset HDP, regardless of whether it is diagnosed antepartum, intrapartum, or postpartum, is associated with an increased risk of incident hypertension 2-7 years after delivery, compared with individuals without HDP during their first birth. Greater awareness of cardiovascular disease risk after HDP-even when HDP is diagnosed during labor or postpartum-is needed to appropriately risk stratify and help prevent hypertension after delivery. ClinicalTrials.gov, NCT02231398.

The relationship between the neurodevelopment in infants exposed to maternal Type-1 diabetes and changes in fetal DNA methylation has not yet been investigated. This hypothesis-generating study, we aimed to determine whether neurodevelopmental outcomes in offspring from mothers with Type-1 diabetes are associated with intrauterine epigenetic changes in fetal DNA. We conducted a prospective, pilot case-control study, comparing infants exposed to maternal Type-1-diabetes with control infants. Cord blood DNA samples were analyzed using the TruSeq-Methyl-Capture-EPIC-Kit, covering over 3.3 million CpGs. The Bayley-III Scales were used to assess infant neurodevelopment, and the scores were correlated with the newborn DNA methylation data. In infants exposed to maternal diabetes, we identified 108 differentially methylated genes enriched in pathways crucial for neurodevelopment: Vocal, Imitative and Observational Learning, Synapse Organization, and Neurogenesis. The greatest methylation differences were observed in differentially methylated regions (DMRs) annotated to key neurological genes: MYT1L (21.61%, q=1.97E-07), NRXN1 (12.30%, q=5.04E-75), SHANK3 (11.62%, q=9.81E-06) and KIRREL3 (7.35%, q= 1.53E-23). Both, NRXN1 and SHANK3, were enriched across all identified neurodevelopmental pathways. At two years of age, the infants exposed to maternal Type-1 diabetes scored significantly lower on the Bayley-III Scales across the cognitive, language, and motor domains. Methylation values across loci annotated to ten neurodevelopment-associated genes were linked to Bayley-III cognitive, language, and/or motor domain scores-with MYT1L and NRXN1 showing significant correlation with the Bayley-III language domain score. While further confirmation is needed, we provide the first results supporting the hypothesis that neurodevelopmental alterations observed in offspring of mothers with Type-1 diabetes are potentially associated with DNA methylation changes during intrauterine life which can be identified at birth.

Evidence on the association between maternal diabetes and neurodevelopmental disorders in offspring, particularly epilepsy, remains limited and heterogeneous. Moreover, most studies have not distinguished among diabetes subtypes-type 1 (T1DM), type 2 (T2DM), and gestational diabetes mellitus (GDM)-which have distinct etiologies. This study examines the association among these diabetes subtypes and epilepsy in offspring. In a retrospective birth cohort of all in-hospital live births between 2002 and 2018 in Ontario, Canada's most populous province, linked with population maternal and child health records up until March 2020, we estimated the crude and adjusted association among T1DM, T2DM, and GDM and epilepsy in children aged younger than 18years using Cox proportional hazards models. We examined the robustness of results using quantitative bias analyses. Among 2 105 553 children, 160 644 (7.6%) were exposed to maternal diabetes (0.3% T1DM, 1.2% T2DM, and 6.1% GDM). Over a median follow-up of 10.2years, 17 853 epilepsy cases were diagnosed. After adjusting for maternal socioeconomic and clinical characteristics, children exposed to maternal diabetes had an increased risk of epilepsy in all subcategories of diabetes compared with those unexposed (adjusted HR [aHR] for T2DM, 1.40; 95% CI, 1.24-1.58; aHR for T1DM, 1.32; 95% CI, 1.03-1.69; and aHR for GDM, 1.14; 95% CI, 1.07-1.22). A longer duration of T1DM or T2DM was associated with an increased risk. These results were consistent in our quantitative bias analyses. Maternal diabetes, particularly T1DM and T2DM, is associated with an increased epilepsy risk in offspring, with longer disease duration not significantly amplifying this risk. These findings suggest that prenatal metabolic and inflammatory exposures may contribute to the development of epilepsy.

To assess temporal trends in outcomes of pregnancies with maternal or paternal type 1 diabetes compared to the general population. Register-based study. Denmark. 1 551 893 pregnancies from 1997 to 2021, hereof 5478 with maternal and 8072 with paternal type 1 diabetes. Crude and adjusted logistic regression analyses allowing for interaction between diabetes and time compared outcomes of pregnancies with maternal or paternal type 1 diabetes to the general population and evaluated temporal trends over a 25-year period. Hypertensive disorders of pregnancy, caesarean delivery, preterm delivery (< 37-week gestation), very preterm delivery (< 34-week gestation), large for gestational age (LGA) (birth weight > 90th percentile) and extreme LGA (birth weight > 97.5th percentile). We observed an increasing prevalence of maternal (0.3%-0.4%) and paternal (0.5%-0.6%) diabetes during the study period. From 1997-2001 to 2017-2021, pregnancies with maternal diabetes had decreasing odds of preterm delivery (aOR 0.62, 95% CI 0.51;0.74), very preterm delivery (aOR 0.62, 95% CI 0.44;0.87) and extreme LGA (aOR 0.73, 95% CI 0.61;0.88) but remained associated with higher odds of each considered pregnancy outcome in both first and last period (aOR 3.59-18.86) compared to the general population. Pregnancies exposed to paternal diabetes were comparable to the general population. Despite a decline in adverse outcomes in pregnancies with maternal type 1 diabetes over the last 25 years, the odds remain greatly increased. These findings support a predominant role of maternal diabetes management rather than parental diabetes genes for pregnancy outcomes.

Maternal hypothyroidism and diabetes alter plasma concentration and placental signaling of sex steroids in rats.

The link between maternal diabetes and congenital heart defects is well-established; however, few studies have investigated subclinical cardiovascular dysfunction at birth, which may serve as an early indicator of future risk. We analyzed cardiovascular metrics, including heart rate and blood pressure during the postnatal hospital stay, in 1927 maternal-infant dyads at Nebraska Medicine (2012-2023), including 226 with gestational diabetes mellitus (GDM), 27 with type 1 DM (T1DM), 67 with type 2 DM (T2DM), and 1607 with no DM. Relationships between maternal diabetes subtype and neonatal cardiovascular metrics were examined using treatment effects modeling. Correlations between maternal glycemic burden, as assessed by average HbA1c and 1-hour oral glucose tolerance test (OGTT) during pregnancy, and newborn cardiovascular metrics were also evaluated. Compared with no DM, T1DM was associated with higher newborn systolic blood pressure (SBP) (+4.6 mm Hg, p = 0.002), pulse pressure (PP) (+3.1 mm Hg, p = 0.006), and SBP variability (+1.2 mm Hg, p = 0.048). T2DM was associated with higher newborn SBP (+2.9 mm Hg, p = 0.03) and PP (+2.0 mm Hg, p = 0.02) and lower SBP variability (-1.3 mm Hg, p = 0.049). There were sigsnificant positive correlations between maternal HbA1c and newborn heart rate (p = 0.009, R 2 = 0.27), mean arterial pressure (p = 0.004, R 2 = 0.20), SBP (p < 0.001, R 2 = 0.22), diastolic BP (p = 0.03, R 2 = 0.17), and PP (p = 0.001, R 2 = 0.17). No correlations were observed between maternal 1-hour OGTT and newborn cardiovascular metrics. These findings indicate early subclinical changes in cardiovascular physiology in offspring of women with DM. The differential impacts of diabetes subtypes on newborn BP and strong link to maternal glycemic burden suggest severity and timing of maternal diabetes influence neonatal cardiovascular physiology.

Maternal endometriosis: An independent risk factor for long-term infectious morbidity of the offspring.