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Gestational diabetes mellitus (GDM) presents significant risks during pregnancy, including adverse perinatal outcomes and placental dysfunction. Impaired angiogenesis, involving crucial factors like Vascular Endothelial Growth Factor (VEGF), contributes to these complications. The Nrf2/Keap1 pathway, crucial for vascular redox homeostasis, has been linked to GDM-associated angiogenesis dysregulation. This study aimed to investigate the molecular mechanisms underlying placental Nrf2 regulation, focusing on angiomiRs, key regulators of angiogenesis in GDM. Computational analysis identified miR-142-5p targeting Nrf2 mRNA. Expression levels of miR-142-5p were assessed in GDM placenta and correlated with Nrf2 expression. Experimental validation utilized human trophoblastic cell lines (BeWo) exposed to hyperglycemic conditions, assessing the effects of anti-miR-142 transfection on Nrf2 expression and angiogenic marker levels. miR-142-5p expression was significantly downregulated in GDM placenta, correlating positively with Nrf2 expression. In BeWo cells exposed to hyperglycemia, anti-miR-142 transfection notably increased Nrf2 expression alongside angiogenic marker levels, confirming the computational predictions. Our findings highlight the pivotal role of miRNAs in GDM-associated impaired angiogenesis by modulating Nrf2 expression. Understanding these molecular mechanisms provides insights into potential therapeutic targets for improving pregnancy outcomes in GDM cases. • Nrf2, its downstream targets and angiogenic factors were downregulated in GDM placenta. • Overexpression of miR-142-5p impairs angiogenesis via dysregulation of Nrf2 in GDM. • MiR-142-5p directly binding with functional domains of Nrf2 in silico. • Silencing miR-142-5p restores Nrf2 and angiogenesis expression in HG induced BeWo cells. [ABSTRACT FROM AUTHOR]

Gestational diabetes mellitus (GDM) is a common condition in pregnancy, the prevalence of which has increased. Identifying modifiable risk factors for GDM, such as dietary factors, could prevent or delay the onset of the condition. Our goal was to perform a comprehensive meta-analysis of cohort studies, to summarize the current evidence on the relationship between total, animal, and plant protein intake during pregnancy, as well as pre-pregnancy protein intake, and the risk of GDM. A literature search was completed using Scopus, PubMed, Web of Science, and Google Scholar up to January 2023 and references of retrieved relevant articles. Observational studies examining the association between the consumption of dietary protein from different sources in pre-pregnancy or/and during pregnancy and the risk of GDM were included. To combine effect sizes for the comparison between the highest and lowest categories of protein intake, a random effects model was utilized. Dose–response relationships were investigated using a 1-stage random-effects model. 8 observational studies were included in the systematic review and 5 prospective cohort studies in the meta-analysis, involving a total of 24,160 participants and 2450 cases of GDM. The analysis revealed a significant association between total protein intake during pregnancy and an elevated risk of GDM (relative risk (RR): 2.24, 95 % confidence interval (CI): 1.67–3.00, P = 0.000). Conversely, no significant association was found between total protein intake before pregnancy and the risk of GDM. Both animal protein intake before pregnancy (RR: 1.47, 95 % CI: 1.06–2.03, P = 0.021) and during pregnancy (RR; 2.31, 95 % CI: 1.43–3.73, P = 0.001) showed a significant association with GDM. Interestingly, there was no significant association between the consumption of plant protein both before and during pregnancy and the risk of GDM. Further analysis revealed that an additional 5 % energy from total protein and animal protein per day was associated with a 24 % and 32 % before and 114 % and 67 % increased risk of GDM during pregnancy respectively. In conclusion, consumption of animal protein and total protein before pregnancy is associated with an increased risk of GDM, although the association is not significant for total protein. Conversely, plant protein intake is linked to a decreased risk of GDM, however, the results are not significant. The intake of any protein type (plant/animal/total) during pregnancy is associated with an elevated risk of GDM, with this association being statistically insignificant for plant protein. Further cohort studies are required to validate the findings presented in this study. PROSPERO (CRD42023396215). [ABSTRACT FROM AUTHOR]

Models of care for women with gestational diabetes mellitus (GDM) have evolved in an ad hoc way and do not meet women's needs. GDM affects 50,000 Australian women per annum with prevalence quadrupling in the last ten years. Many health services are struggling to provide a quality service. People with diabetes are calling for care that focuses on their wellbeing more broadly. To examine the holistic (emotional, social, economic, and spiritual) care needs of women with GDM. Qualitative and mixed-methods studies capturing the healthcare experiences of women with GDM were searched for in CINAHL, Medline, Web of Science and Scopus. English-language studies published between 2011 and 2023 were included. Quality of studies was assessed using Crowe Critical Appraisal Tool and NVIVO was used to identify key themes and synthesise data. Twenty-eight studies were included, representing the experiences of 958 women. Five themes reflect women's holistic needs through their journey from initial diagnosis to postpartum: psychological impact, information and education, making change for better health, support, and care transition. The biomedical, fetal-centric model of care neglects the woman's holistic wellbeing resulting in high levels of unmet need. Discontinuity between tertiary and primary services results in a missed opportunity to assist women to make longer term changes that would benefit themselves (and their families) into the future. The provision of holistic models of care for this cohort is pivotal to improving clinical outcomes and the experiences of women with GDM. [ABSTRACT FROM AUTHOR]

We investigated the proinflammatory functions of endoplasmic reticulum stress and peroxisome proliferator-activated receptor α (PPARα) in the development of gestational diabetes mellitus (GDM) and their relationship in regulating inflammation in GDM. This study was performed on placentas of normal pregnant women, women with GDM, and HTR8 cells. Transmission electron microscopy, immunohistochemistry, Western blot analysis, and RT-PCR were performed to analyze ERS and PPARα expression on both normal and GDM pregnancy placentas. ELISA was performed to analyze inflammatory biomarkers. To generate models of the GDM-like state, placentas of normal pregnancy were treated with LPS and polyinosinic-polycytidylic acid (poly [I:C]). TG, CHOP plasmid, and CHOP siRNA were assessed as to their regulation of HTR8 cells to discern the relationship between ERS and PPARα in regulating the inflammation associated with GDM. ERS was elevated in GDM placentas, induced the secretion of IL-6 and TNF-α, and attenuated the expression of GLUT-4. PPARα was diminished in GDM placentas and inhibited the inflammatory responses via the NF-κB nuclear-transport process. 4-PBA reduced CHOP and augmented PPARα, and it decreased IL-6 and TNF-α in our GDM-like explant. However, with both 4-PBA and MK886 treatment, we noted no significant difference in CHOP expression. The level of PPARα was reduced, and that of NF-κB p65 in the nucleus was elevated with TG treatment in the HTR8/Svneo. Knockdown of CHOP increased PPARα and reduced NF-κB p65, while expression of PPARα declined, and that of NF-κB p65 rose with the application of CHOP when HTR8 cells were treated with TG. ERS contributes to the pathophysiology of GDM in pregnancy via the CHOP-PPARα–NF–κB-signalling pathway by inducing aberrant activation of inflammation and insulin resistance. • ERS is increased including CHOP and induced pro-inflammatory function in GDM placentas. • PPARα is downregulated and promotes the NF-κB nuclear-transport process in placental of GDM. • Regulation of ERS affects the expression of pro-inflammatory factors through CHOP-PPARα–NF–κB pathway in GDM. [ABSTRACT FROM AUTHOR]

• Associations of common genetic risk variants with GDM risk in the north Indian population were investigated. • Relative risk, population penetrance and attributable risk for risk allele variants was higher in GDM mother. • Four variants FTO, PPARG2, SLC30A8, and TCF7L2 were significantly associated with BMI, HbA1c and insulin. • Four variants FTO, PPARG2, SLC30A8, and TCF7L2 were significantly associated with GDM in North Indian population. The current study sought to investigate the associations of common genetic risk variants with gestational diabetes mellitus (GDM) risk in the north Indian population and to evaluate their utility in identifying GDM cases. A case-control study, including 300 pregnant women, was included, and clinical and pathological information was collected. The amplification-refractory mutation system (ARMS) was used for genotyping four single nucleotide polymorphisms (SNPs), namely FTO (rs9939609), PPARG2 (rs1801282), SLC30A8 (rs13266634), and TCF7L2 (rs12255372). The odds ratio and confidence interval were determined for each SNP in different genetic models. Further, attributable risk, population penetrance, and relative risk were also calculated. The risk allele A of FTO (rs9939609) poses a two times higher risk of GDM (p = 0.02, OR = 2.5). The CG and GG genotypes of PPARG2 (rs1801282) have half a lower risk of GDM. In SLC30A8 (rs13266634), the recessive model analysis showed a two times higher risk of having GDM, while the recessive model (TT vs. GG + GT) analysis in TCF7L2 (rs12255372) indicates a lower risk of GDM. Finally, the relative risk, population penetrance, and attributable risk for risk allele in all four variants was higher in GDM mothers. All four polymorphisms were found to be significantly associated with BMI, HbA1c, and insulin. Our study first time confirmed a significant association with GDM for four variants, FTO, PPARG2, SLC30A8, and TCF7L2, in the North Indian population. [ABSTRACT FROM AUTHOR]

• Gut microbiota dysfunction promotes the GDM process. • The gut microbiota participates in lipids metabolism in intestine. • Intestinal flora derived SCFA involve in lipid transport. • Fecal microbiota transplantation from GDM pregnant women promotes GDM process in mice. Gut flora is considered to modulate lipid transport from the intestine into the bloodstream, and thus may potentially participate in the development of GDM. Although previous studies have shown that the intestinal microbiota influences lipid transport and metabolism in GDM, the precise mechanisms remain elusive. To address this, we used a high-fat diet (HFD)-induced GDM mouse model and conducted 16s rRNA sequencing and fecal metabolomics to assess gut microbial community shifts and associated metabolite changes. Western blot, ELISA, and chromatin immunoprecipitation (ChIP) were utilized to elucidate how gut microbiota affect intestinal lipid transport and the insulin sensitivity of hepatic, adipose, and skeletal muscle tissues. We found that HFD impaired the oral glucose tolerance test (OGTT) and insulin tolerance test (ITT) in pregnant mice. 16s rRNA sequencing demonstrated profound compositional changes, especially in the relative abundances of Firmicutes and Bacteroidetes. Metabolomics analysis presented a decline in the concentration of short-chain fatty acids (SCFAs) in the GDM group. Western blot analyses showed an upregulation of HDAC3 and a concurrent reduction in H3K27 acetylation in the intestine. ChIP-qPCR showed that PPAR-γ was inhibited, which in turn activated lipid-transporter CD36. ELISA and insulin signaling pathway detection in insulin-target organs showed high concentrations of circulating fatty acids and triglycerides and insulin resistance in insulin-target organs. Our results suggest that gut microbiota is closely associated with the development of GDM, partly because decreased gut flora-associated SCFAs activate CD36 by suppressing the HDAC3-H3K27ac-PPAR-γ axis to transport excessive fatty acids and triglycerides into blood circulation, thereby dysregulating the insulin sensitivity of insulin target organs. [ABSTRACT FROM AUTHOR]

Ever since the Gravity Driven Membrane (GDM) system was proposed in 2010 as an environmentally friendly and low-carbon water treatment technology, the search for an appropriate pre-treatment measure to combat the low stable flux and membrane fouling has been of great importance for the promotion and development of GDM systems. This review summarized the effects of pre-treatment measures (particulate adsorption, coagulation, oxidation) in existing reports on stable flux, membrane fouling and water quality of GDM systems. Based on the literature reports, the internal mechanism was classified. The effects of different pretreatment conditions on stable flux were evaluated by meta-analysis, and the optimal process conditions to maintain higher stable flux with different pretreatments were predicted. The analysis revealed that appropriate pretreatment selection could improve the performance of the GDM system by removing fouling by the pretreatment itself, reducing bacterial EPS emissions, producing smaller/more hydrophilic pollutant molecules, enhancing bioactivity and generating a looser membrane structure. Moreover, the investment and operating costs of GDM systems can be reduced through suitable pre-treatment measures, thereby expanding their application in decentralized water supply and wastewater treatment. Given the variability and uniqueness of water source conditions, this review aimed to guide the design of pretreatment measures in GDM systems to improve the efficiency of targeted treatment and promote its applicability. [Display omitted] • Collect and re-analyze pretreatment measures with meta-analysis. • Pretreatment location affects GDM system performance. • Pretreatment enables targeted removal of pollutants by GDM systems. • Preprocessing can reduce GDM system cost. [ABSTRACT FROM AUTHOR]

Introduction: The purpose of the present study was to compare maternal serum betatrophin levels during the first trimester from healthy pregnancies to those complicated by gestational diabetes mellitus (GDM).Methods: In this prospective study, 320 pregnant women were evaluated in their first trimester, and 145 pregnant women who met the inclusion criteria were divided into the following two groups according to GDM screening results: GDM (n:20) and non-diabetic healthy control (n: 125). Samples of maternal serum fasting insulin, fasting blood glucose, hemoglobin (HB)A1c, and betatrophin levels obtained from the women's blood samples between 11+0/7 -13+6/7 gestational weeks during first trimester nuchal translucency screening. 75-g oral glucose tolerance test protocol was preferred for GDM scanning between 24+0/7 -28+0/7 gestational weeks.Results: Maternal age and first-trimester body mass index (BMI) were higher in the GDM group than in the control group. Gestational age at blood draw was similar between the groups. First-trimester fasting insulin, fasting glucose, hemoglobin (Hb)A1c, thyroid-stimulating hormone, triiodothyronine (sT3), and thyroxine (sT4) were statistically similar between groups. First trimester Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) was 2.67 ± 1.42 in the GDM group and 2.12 ± 1.61 in the control group and not statistically different. Maternal age and BMI adjusted first-trimester maternal serum betatrophin levels were 11.58 ± 6.40 ng/mL in the GDM group and 31.11 ± 3.00 ng/mL in the control group and was statistically lower in the GDM group (p < 0.001).Discussion: Our results indicated that first trimester maternal serum betatrophin levels are decreased in pregnancies complicated by GDM and first trimester betatrophin levels could be an early screening tool for GDM to allow better pregnancy management. [ABSTRACT FROM AUTHOR]

Polycyclic aromatic hydrocarbons and phthalate acid esters (PAHs & PAEs), known as endocrine disrupting chemicals (EDCs), widely exist in daily life and industrial production. Previous studies have suggested that PAHs & PAEs may modify the intrauterine homeostasis and have adverse effects on fetal development. However, epidemiological evidence on the associations between PAHs & PAEs and gestational diabetes mellitus (GDM) is still limited. To investigate the effects of prenatal PAHs &PAEs exposure on the risk of GDM and hyperglycemia in pregnant women. The study population was a total of 725 pregnant women from a prospective birth cohort study conducted from December 2019 to December 2021. Blood glucose levels were collected by the hospital information system. Urinary PAHs & PAEs concentrations were determined by gas chromatography tandem mass spectrometry. The Poisson regression in a generalized linear model (GLM), multiple linear regression, quantile-based g-computation method (qgcomp), and Bayesian kernel machine regression (BKMR) were applied to explore and verify the individual and overall effects of PAHs & PAEs on glucose homeostasis. Potential confounders were adjusted in all statistical models. A total of 179 (24.69%) women were diagnosed with GDM. The Poisson regression suggested that a ln-unit increment of 4-OHPHE (4-hydroxyphenanthrene) (adjusted Risk Ratio (aRR) = 1.13; 1.02–1.26) was associated with the increased GDM risk. Mixed-exposure models showed similar results. We additionally found that MBZP (mono-benzyl phthalate) (aRR = 1.19; 1.02–1.39) was positively related to GDM risk in qgcomp model. Although neither model demonstrated that 2-OHNAP (2-hydroxynaphthalene) and 9-OHFLU (9-hydroxyfluorene) increased the risk of GDM, 2-OHNAP and 9-OHFLU exposure significantly increased blood glucose levels. BKMR model further confirmed that overall effects of PAHs & PAEs were significantly associated with the gestational hyperglycemia and GDM risk. Our study presents that environmental exposure to PAHs & PAEs was positively associated with gestational glucose levels and the risks of developing GDM. In particular, 2-OHNAP, 9-OHFLU, 4-OHPHE and MBZP may serve as important surveillance markers to prevent the development of GDM. • This is the first and largest cohort study to explore the association between PAHs & PAEs and GDM incidence. • Exposure to PAHs & PAEs mixtures was positively associated with higher GDM risk and gestational blood glucose levels. • BKMR and qgcomp were employed to adapt to the complexity of mixed exposures. • 2-OHNAP, 9-OHFLU, 4-OHPHE, and MBZP were major contributors to disturbing gestational glucose homeostasis. [ABSTRACT FROM AUTHOR]

Gestational diabetes mellitus (GDM) is a pregnancy-specific disease characterized by impaired glucose tolerance during pregnancy. Although diagnosis and clinical management have improved significantly, there are still areas where therapeutic approaches need further improvement. Recent evidence suggests that CCL2, a chemokine involved in immunoregulatory and inflammatory processes, is closely related to GDM. However, the potential value for clinical therapeutic applications and the mechanism of CCL2 in adipose tissue macrophages (ATMs) of GDM remain to be elucidated. Here, we found that CCL2 was enriched in macrophages of the visceral adipose tissue from GDM women and HFD-induced GDM mice. The combination of in vitro and in vivo experiments showed that Ccl2 silencing inhibited the inflammatory response of macrophage by blocking calcium transport between ER and mitochondria and reducing excessive ROS generation. Additionally, the ATS-9R/siCcl2 oligopeptide complex targeting adipose tissue was created. Under the delivery of ATS-9R peptide, Ccl2 siRNA is expressed in ATMs, which reduces inflammation in adipose tissue and, as a result, mitigates insulin resistance. All of these findings point to the possibility that the ATS-9R/siCcl2 complex, which targets adipose tissue, is able to reduce insulin resistance in GDM and the inflammatory response in macrophages. The ATS-9R/siCcl2 oligopeptide complex targeting adipose tissue seems to be a viable treatment for GDM pregnancies. [Display omitted] • ATS-9R delivers Ccl2 siRNA specifically to adipose tissue macrophages. • Ca2+ dependent mitochondrial ROS is reduced in Ccl2 silenced adipose tissue macrophages. • ATS-9R/siCcl2 complexes inhibit inflammatory response of adipose tissue macrophage. • ATS-9R/siCcl2 complexes benefit improving insulin resistance in GDM. [ABSTRACT FROM AUTHOR]

Background and Aims: Previous literature have shown a diversity of findings regarding the relationship between the maternal gut microbiota and gestational diabetes mellitus (GDM). We investigated the gut microbiota of overweight and obese women with gestational diabetes mellitus (GDM) against matched euglycaemic women at 16 and 28-weeks' gestation.Methods and Results: This study included women from the SPRING (Study of PRobiotics IN Gestational diabetes) cohort. Overweight and obese women with no impaired glucose tolerance or impaired fasted glucose were enrolled prior to gestational age <16 weeks. Participants with a diagnosis of GDM (n = 29) were matched with euglycaemic (n = 29) women for body mass index, probiotic or placebo intervention, maternal age, parity and ethnicity. Anthropometric, clinical and fecal microbiota (16S rRNA amplicon-based sequencing of V6-V8 region) data was assessed at 16 and 28-weeks' gestation. The relative abundances of key bacterial genera were not significantly altered between euglycaemic women and women with GDM. Occurrence of bacterial taxa was similar between groups at both timepoints. GDM was associated with decreased Shannon diversity (p = 0.02) without differentiated clustering measured by beta diversity at 28-weeks' gestation.Conclusions: Overweight and obese women with GDM demonstrate minor variation in the gut microbiota at 16 and 28-weeks' gestation compared with matched euglycaemic women. This study expands on previous literature concluding the microbiota does not likely have a disease-specific characterisation in GDM. [ABSTRACT FROM AUTHOR]

Objective: Gestational diabetes mellitus (GDM) is defined as any degree of glucose intolerance which is diagnosed during pregnancy and poses considerable health risks for mother and child. Maternal body mass index (BMI) correlates with GDM diagnosis and the pathophysiology of this link may be explained through oxidative stress and mitochondrial dysfunction. In this study we investigate if mitochondrial dysfunction is evident in GDM by measuring cell free mitochondrial DNA concentration and determine if a potential relationship exists between maternal mitochondrial function and GDM diagnosis.Study Design: Plasma samples were taken at 20 weeks' gestation from women who subsequently developed GDM (n = 44) and matched with women with uncomplicated pregnancies (n = 85) as controls. Control group 1 was matched by maternal age and BMI (n = 41) to GDM cases, while control group 2 was matched by maternal age alone (n = 44). Prediction potential was determined by binary regression analysis. Statistical analysis was performed on SPSS Statistics v25.Results: Binary regression analysis showed a statistically significant association between mtDNA concentration and GDM diagnosis (p = 0.032) in GDM cases versus control group 2, indicating that GDM patients have higher circulating mtDNA concentrations relative to healthy control patients. The lack of statistical significance in control group 1 suggests that BMI may be linked to mitochondrial function in GDM patients.Conclusion: These results demonstrate a potential pathogenic role for mitochondrial dysfunction in GDM, with BMI presenting as a likely physiological mediator. [ABSTRACT FROM AUTHOR]

Background: The amount of chewing might be relevant in reducing hyperglycaemia in diabetic patients. The study assessed the impact of enhanced chewing on glycaemic control in women with gestational diabetes mellitus (GDM).Methods: As an open-label, mono-centre randomized controlled trial, 59 women with recent diagnosis of GDM were included. They received either routine care or additional chewing gum intervention. SMBG was performed for five days.Results: No significant impact on mean values of postprandial glucose levels were observed. The estimated mean differences (intervention vs. control group) were: 4.9 mg/dl, 98.4 %CI -7.2-17.1 (breakfast); -4.5 mg/dl, 98.4 %CI -15.1-6.0 (lunch); -3.8 mg/dl, 98.4 %CI -15.9 to 8.4 (dinner). OGTT levels at 60 and 120 min. were associated with glucose levels after breakfast.Conclusion: In conclusion, no significant differences in blood glucose levels were observed between the groups and therefore major effects of chewing on hyperglycaemia in women with GDM could be excluded.Trial Registration: ClinicalTrials.gov; NCT03961542, Date of registration: 20.01.2019. Retrospectively registered. [ABSTRACT FROM AUTHOR]

Poor sleep quality is very common among pregnant women. Gestational diabetes mellitus (GDM) has been related to various adverse maternal and neonatal outcomes. The aim of this systematic review was to examine the association between poor sleep quality and gestational diabetes risk. Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, a systematic search was conducted in five electronic databases from inception to February 2019. Studies that examined the relationship between sleep quality and glucose in pregnant women were screened for eligibility. Pooled odds ratio (OR) with 95% confidence interval (CI) was calculated from aggregate data using a fixed-effect model. Thirteen non-experimental studies (n = 21,194 women) were eligible for inclusion. Poor sleep quality was measured using subjective questionnaires in nine studies and objective methods (actigraphy or polysomnography) in four studies. GDM was typically diagnosed following standard guidelines. Eight studies were included in the meta-analysis for GDM. Overall, self-reported poor sleep quality was a significant risk factor for GDM (pooled OR = 1.43, 95%CI: 1.16,1.77, p = 0.001). Three studies examined the association between objective sleep quality and GDM, but no significant relationship was observed. Subjective poor sleep quality was related to an increased risk for GDM, while objectively measured sleep quality was not. This review was limited by the assessment of sleep quality. Future larger studies are warranted to examine the effects of sleep quality on glucose metabolism in pregnancy. Ideally, these studies should measure sleep quality using both validated questionnaires and objective methods. These will provide further directions for improving sleep during pregnancy and exploring its effects on glucose metabolism. [ABSTRACT FROM AUTHOR]

Vitamin D deficiency is prevalent in pregnancy and has been associated with increased occurrences of preeclampsia, cesarean delivery, neonatal bacterial vaginosis, and gestational diabetes. CYP24A1, recognized as a key factor in vitamin D metabolism homeostasis, encodes 24-hydroxylase responsible for converting 25(OH)D3 and 1,25(OH)2D3 into inactive metabolites. Recently, we have reported CYP24A1 overexpression in patients with gestational diabetes mellitus (GDM) and trophoblast cells exposed to hyperglycemia. In this study, we explored miRNA-mediated regulation of CYP24A1 in GDM progression, validating our findings through silencing experiments in a trophoblast cell line. In silico tools identified miR-125b-5p as a putative target of CYP24A1. Expression analysis revealed downregulation of miR-125b-5p in blood samples from early GDM and GDM compared to healthy pregnant women, positively correlating with vitamin D levels. Hyperglycemic exposure in human trophoblastic cell lines (BeWo) decreased miR-125b-5p expression, concomitant with an increase in CYP24A1. To confirm the regulatory role of miR-125b on CYP24A1, we transfected BeWo cells with antimiR-125b or miR-125b mimic. AntimiR-125b transfection heightened CYP24A1 levels, while miR-125b mimic overexpression resulted in decreased CYP24A1 expression. These findings establish miR-125b as a regulator of CYP24A1. To explore the influence of miR-125b on vitamin D metabolism, trophoblast cells overexpressing miR-125b were treated with 0.1 and 1 µM calcitriol. Hyperglycemic conditions exhibited a reduction in CYP24A1 levels. Collectively, our results indicate that miR-125b may regulate vitamin D metabolism by targeting CYP24A1, contributing to GDM progression. These findings may pave the way for understanding vitamin D resistance in concurrent GDM development and identifying novel miRNAs targeting CYP24A1. • Overexpression of CYP24A1 in gestational diabetes mellitus (GDM) patients and hyperglycemia-exposed trophoblast cells. • miR-125b-5p downregulation was observed in blood samples from early GDM and GDM patients compared to healthy pregnant women. • Hyperglycemic exposure in trophoblast cells results in decreased miR-125b-5p expression and increased CYP24A1 expression. • Transfection experiments confirm the regulatory role miR-125b on CYP24A1 expression. • Cells overexpressing miR-125b-5p shows reduction in CYP24A1 levels under hyperglycemic condition. [ABSTRACT FROM AUTHOR]

We consider as discretization in space, the GDM (Gradient Discretization Method) developed recently in Droniou et al. (2018), to approximate multidimensional time fractional diffusion and diffusion-wave equations where the fractional order α of the time derivative is respectively satisfying 0 < α < 1 and 1 < α < 2. The time fractional derivative is given in the Caputo sense. The time discretization is performed using a uniform mesh. For the time fractional diffusion equation, we derive an implicit scheme. In addition to an L ∞ (L 2) -a priori estimate, which can be derived from a reasoning in Bradji (2018), we present and prove a new L 2 (H 0 1) -a priori estimate for the discrete problem. Under the assumption that the exact solution is sufficiently smooth, these a priori estimates allow to prove error estimates in discrete norms of L 2 (H 0 1) and L ∞ (L 2). The convergence order in these estimates is optimal in the sense of two points of view. The first one is that the order in space is the same one proved in Droniou et al. (2018) for elliptic equation, whereas the second point of view is that the particular case of this order when α = 1 is the same one obtained in Droniou et al. (2018) for the standard heat equation. For the time fractional diffusion-wave equation, we derive two implicit schemes. A full convergence analysis is carried out for both schemes. In particular, we develop new a priori estimates which yield error estimates in several discrete norms for each scheme. The convergence is proved to be unconditional and optimal. The convergence results are obtained thanks to a comparison with appropriately chosen auxiliary gradient schemes and to the stated a priori estimates. These results improve the ones of Bradji (2017) in which a conditional convergence is proved for a SUSHI (Scheme using Stabilization and Hybrid Interfaces) approximating a time-fractional diffusion-wave equation. For both cases of time fractional diffusion and diffusion-wave equations, we show the well-posedness in the sense that the discrete solutions depend continuously on the data of the considered problems. The stated results can be extended to multi-term time-fractional diffusion and diffusion-wave equations. One of the main features when using GDM is that their results hold for all the schemes within the framework of GDM: conforming and nonconforming finite element, mixed finite element, hybrid mixed mimetic family, some Multi-Point Flux approximation finite volume schemes, and some discontinuous Galerkin schemes. Some examples of schemes recovered by the GSs (Gradient Schemes) presented in this work are sketched. Among these examples, we quote the one presented in Jin et al. (2015) to approximate time fractional diffusion equations. This work extends and improves some results presented in brief or stated without proof in the notes Bradji (2018). We present some numerical tests using SUSHI introduced in Eymard et al. (2010) to support the theoretical results. [ABSTRACT FROM AUTHOR]

To elaborate how the viral load of HBV affects the gestational diabetes mellitus (GDM). We enrolled 196 chronic HBV-infected pregnant patients in this hospital between January 2012 and December 2017 for delivery in this study. According to the viral load of HBV-DNA, these patients were divided into the HBV-DNA negative group (n = 107, <1 × 103 copies/mL) and HBV-DNA positive group (n = 89, ≥1 × 103 copies/mL). Simultaneously, 100 HBV-free pregnant women who were admitted to the hospital for delivery were included in the control group. Before delivery, fasting venous blood was drawn from the pregnant women to perform the HBV-DNA quantification through qRT-PCR; from the 24th to 28th gestation week, all pregnant women underwent OGTT, with the third-trimester-of-pregnancy as the endpoint. Besides, we also measured the FBG, 2hPG and hemoglobin A1c (HbAIc). Among 168 pregnant patients carrying chronic HBV, viral load of 107 patients was less than 1 × 103 copies/mL (54.6%), and 89 not less than 1 × 103 copies/mL (45.4%). The incidence rates of GDM in the HBV-DNA negative group and HBV-DNA positive group were 18.7% and 19.1%, respectively, significantly higher than that in the control group (p < 0.05), while the difference of the incidence rates of GDM between two HBV-DNA groups were not significant (p > 0.05). In HBV-DNA negative group and HBV-DNA positive group, FBGs, 2hPGs and HbAIcs were respectively (6.96 ± 0.36) mmol/L and (7.04 ± 0.37) mmol/L, (10.26 ± 1.29) mmol/L and (10.16 ± 1.12) mmol/L, and (8.66 ± 0.97) % and (8.91 ± 0.90) %, significantly higher than (4.57 ± 0.34) mmol/L, (6.16 ± 0.86) mmol/L and (5.13 ± 0.57) % (p < 0.05); however, between two HBV-DNA groups, comparisons of the FBG, 2hPG and HbAIc suggested no significant differences (p > 0.05). In 196 patients carrying chronic HBV, positive correlations were identified between the viral load of HBV-DNA, and FBG, 2hPG and HbAIc (p < 0.01). HBV infection can increase the incidence rate of GDM, and the viral load of HBV-DNA is correlated with the glucose level of pregnant patients. [ABSTRACT FROM AUTHOR]

Biomonitoring studies have shown the presence of structurally diverse perfluoroalkyl acids (PFAAs) in humans but only a few studies are available regarding the differential structural effects of PFAAs on human health. The specific association between different structural PFAAs and both gestational diabetes mellitus (GDM) and glucose homeostasis in pregnant women was investigated. A prospective nested case-control study including 439 women was conducted during 2013–2015 in Beijing, China. First trimester maternal serum was collected and analyzed for 25 diverse PFAAs with varying carbon chain lengths, linear/branched isomers and carboxylate or sulfonate functional groups. The analyzed PFAAs were grouped into different exposure variables depending on structure characteristics. GDM cases were diagnosed at 24–28 weeks of gestation and individually matched in a 1:2 ratio to controls. Conditional logistic and linear regression was used to evaluate the association between structurally grouped PFAAs and both GDM risk and glucose homeostasis parameters. Among the 25 PFAAs, 12 perfluoroalkyl carboxylates (PFCAs) and 8 perfluoroalkyl sulfonates (PFSAs) were detected in >55.0% of samples and were respectively grouped into different structural groups. The structural-based effect was observed for PFCAs, where short-chain (C4-C7) PFCAs continuous level was significantly associated with GDM with an estimated odds ratio (OR) of 1.99 (95% CI: 1.29, 3.09), and the multivariable-adjusted ORs (95% CI) of GDM for increasing tertiles of short-chain PFCAs were 1.00 (ref.), 1.82 (0.80, 4.16) and 3.01 (1.31, 6.94), P trend = 0.011. Additionally, increased concentration of short-chain PFCAs was significantly associated with higher postprandial glucose levels (P < 0.05). Non-significant association was observed between structure grouped PFSAs and GDM as well as glucose homeostasis. This investigation suggests a structure-specific association between short-chain PFCAs exposure and both GDM risk and impaired glucose homeostasis in pregnant women. These findings warrant further investigation with larger samples and a wide range of short-chain PFCAs exposure. • A prospective nested case-control study was conducted. • In total of 25 PFAAs were measured and grouped into different exposure variables. • The specific association between different structural PFAAs and GDM was investigated. • Positive association was found between short-chain PFCAs (C4-C7) and GDM. • Short-chain PFCAs exposure was associated with impaired glucose homeostasis. [ABSTRACT FROM AUTHOR]

The role of inflammasomes in gestational diabetes mellitus (GDM) has emerged as a critical area of research in recent years. Inflammasomes, key components of the innate immune system, are now recognized for their involvement in the pathogenesis of GDM. Activation of inflammasomes in response to various triggers during pregnancy can produce pro-inflammatory cytokines, such as interleukin-1β (IL-1β) and interleukin-18 (IL-18), contributing to systemic inflammation and insulin resistance. This dysregulation not only impacts maternal health but also poses significant risks to fetal development and long-term health outcomes. Understanding the intricate interplay between inflammasomes and GDM holds promise for developing novel therapeutic strategies and interventions to mitigate the adverse effects of this condition on both mothers and their offspring. Researchers have elucidated that targeting inflammasomes using anti-inflammatory drugs and compounds can effectively reduce inflammation in GDM. Furthermore, the addition of nuclear factor erythroid 2-related factor 2 (Nrf2) to this complex mechanism opens novel avenues for therapeutics. The antioxidant properties of Nrf2 may potentially suppress inflammasome activation in GDM. This comprehensive review investigates the intricate relationship between inflammasomes and GDM, emphasizing the pivotal role of inflammation in its pathogenesis. It also sheds light on potential therapeutic strategies targeting inflammasome activation and explores the role of Nrf2 in mitigating inflammation in GDM. • Excessive inflammasome activation plays a pivotal role in the pathogenesis of GDM and its associated complications. • NLRP3-mediated chronic, low-grade inflammation exacerbates both insulin resistance and endothelial dysfunction in GDM. • Dysregulation of the interplay between Nrf2 and the inflammasome pathway is evident in the context of GDM. • Exploring the therapeutic potential of compounds that target inflammasomes and the Nrf2-NLRP3 axis holds promise for the effective management of GDM. [ABSTRACT FROM AUTHOR]

Exposure to gestational diabetes mellitus (GDM) during pregnancy has significant consequences for the unborn baby and newborn infant. However, whether and how GDM exposure induces the development of neonatal brain hypoxia/ischemia-sensitive phenotype and the underlying molecular mechanisms remain unclear. In this study, we used a late GDM rat model induced by administration of streptozotocin (STZ) on gestational day 12 and investigated its effects of GDM on neonatal brain development. The pregnant rats exhibited increased blood glucose levels in a dose-dependent manner after STZ administration. STZ-induced maternal hyperglycemia led to reduced blood glucose levels in neonatal offspring, resulting in growth restriction and an increased brain to body weight ratio. Importantly, GDM exposure increased susceptibility to hypoxia/ischemia (HI)-induced brain infarct sizes compared to the controls in both male and female neonatal offspring. Further molecular analysis revealed alterations in the PTEN/AKT/mTOR/autophagy signaling pathway in neonatal male offspring brains, along with increased ROS production and autophagy-related proteins (Atg5 and LC3-II). Treatment with the PTEN inhibitor bisperoxovanadate (BPV) eliminated the differences in HI-induced brain infarct sizes between the GDM-exposed and the control groups. These findings provide novel evidence of the development of a brain hypoxia/ischemia-sensitive phenotype in response to GDM exposure and highlight the role of the PTEN/AKT/mTOR/autophagy signaling pathway in this process. • STZ-induced maternal hyperglycemia (GDM) decreases neonatal offspring blood glucose levels. • Prenatal exposure to GDM produces a growth restriction and asymmetrical brain development. • GDM exposure causes alterations in the PTEN/AKT/mTOR/autophagy signaling pathway in neonatal offspring. • Prenatal GDM exposure programs a hypoxia/ischemia (HI)-sensitive phenotype of neonatal brain. [ABSTRACT FROM AUTHOR]

Abstract The general dynamic model of oceanic island biogeography (GDM) predicts the immigration, speciation and extinction of terrestrial biota through geological time on oceanic islands. Additionally, the glacial-sensitive model of island biogeography (GSM) also predicts extinction due to eustatic and climate change within islands. However, well-documented and natural pre-Holocene plant extinctions are almost unknown for oceanic islands worldwide. To test these predictions, we have sampled the Early Pleistocene Porto da Cruz lacustrine and fluvial sediments for plant fossils that could confirm the GDM and GSM extinction predictions. Additionally, two new 40Ar/39Ar geochronological analyses were performed, constraining the age of the sediments to 1.3 Ma (Calabrian). Among the fossils, Eurya stigmosa (R.Ludw.) Mai (Theaceae) seeds were recognised and studied by scanning electron microscopy (SEM). E. stigmosa is the first report of a natural (non-anthropogenic) extinct plant in the fossil record for Madeira Island, and for an oceanic island, confirming the GDM and GSM predictions. Eurya spp. palaeobiogeography indicates wider distribution in Europe until the end of the Pliocene (2.58 Ma), becoming extirpated to small refugia and extinct thereafter. The Madeiran record expands the formerly unknown presence of E. stigmosa to the Macaronesian realm. The new dating of the deposit at 1.3 Ma (Calabrian) means that E. stigmosa in Madeira was already in a refugium. The extinction in Madeira is most probably a combination of island ontogeny and climate change due to Pleistocene glaciations. The palaeoecological role of this extinct shrub or tree is currently unknown, but it was a probably an element of the Madeiran laurel forest, as this community was already present in Madeira at least 1.8 My ago. This new information corroborates the predictive power of GDM and GSM and adds a new view on the importance of studying oceanic island palaeobotany, specially palaeocarpofloras. Highlights • Eurya stigmosa (Theaceae) seed fossils are described for Madeira Island (Portugal). • Two new 40Ar/39Ar dates constrain the age of fossils to 1.3 Ma (Calabrian). • Madeira Island acted as a Quaternary refugium for the extirpated European Eurya. • Madeiran Eurya fossils represent a pre-Holocene extinction in an oceanic Island. • Fossils support current oceanic island biogeography models for natural extinctions. [ABSTRACT FROM AUTHOR]

Background: Insulin resistance is common in polycystic ovary syndrome (PCOS). PCOS may be associated with increased risk of gestational diabetes mellitus (GDM).Objectives: To (1) review literature regarding PCOS and hyperglycaemia in pregnancy and (2) present original data from Odense Child Cohort (OCC) regarding GDM in PCOS.Methods: Literature search including original studies from 2000-18. OCC included 2548 pregnant women, 9.5% (n = 241) had PCOS. Fasting plasma glucose was measured in 1519 and 659 oral glucose tolerance tests were performed (with risk factor for GDM, n = 384, without risk factors, n = 275), applying two different GDM criteria.Results: 30 studies were eligible using 12 different sets of diagnostic criteria for GDM. Ten studies included n > 50, control group, assessment of GDM and BMI. Results were not uniform, but supported that higher BMI, higher age, Asian ethnicity, and fertility treatment increased the risk of GDM in PCOS. In OCC, women with PCOS and controls had similar prevalences of GDM independent of different sets of criteria for GDM.Conclusion: PCOS may not be an individual risk factor for GDM. Pregnancies in PCOS are characterized by factors known to increase risk of GDM, especially high BMI and fertility treatment. [ABSTRACT FROM AUTHOR]

Background: Gestational diabetes mellitus (GDM) is a worldwide public health problem. Few studies investigated the association of intra uterine exposure to GDM and long-term endocrine morbidity of offspring.Objective: To assess whether in utero exposure to GDM increases the risk for long-term endocrine morbidity of the offspring.Methods: A retrospective cohort study was conducted including all singleton born to women who delivered between 1988 and 2014. All births occurred in a tertiary medical center. Data were collected from the computerized perinatal database of the obstetrics and gynecology department and the computerized hospitalization database. The exposure variables were: diet-controlled GDM (GDMA1) and treated GDM (GDMA2). Multivariate generalized estimating equation (GEE) logistic regression model analysis was used to control for confounders and for maternal clusters.Results: During the study period 231,271 deliveries met the inclusion criteria, of which 12,642 deliveries (5.4%) were diagnosed with GDM. During the follow-up period, children exposed in utero to GDM had a higher rate of long- term hospitalizations with diagnoses of endocrine morbidity (such as diabetes mellitus and obesity) compared to those unexposed. Using a GEE model, controlling for confounders such as maternal age, follow up-time, obesity and birthweight, in-utero exposure to GDMA1 (adjusted OR = 2.1; 95% CI 1.7-2.7; P < 0.001) and especially to GDMA2 (adjusted OR = 3.1; 95% CI 2.2-4.4, P < 0.001) were found as risk factors for long-term endocrine disease during childhood.Conclusion: Exposure to GDM is a risk factor for long-term endocrine morbidity in the offspring. [ABSTRACT FROM AUTHOR]

Gestational diabetes mellitus (GDM) is associated with excessive oxidative stress which may affect placental vascular function. Cholesterol homeostasis is crucial for maintaining fetoplacental endothelial function. We aimed to investigate whether and how GDM affects cholesterol metabolism in human fetoplacental endothelial cells (HPEC). HPEC were isolated from fetal term placental arterial vessels of GDM or control subjects. Cellular reactive oxygen species (ROS) were detected by H 2 DCFDA fluorescent dye. Oxysterols were quantified by gas chromatography–mass spectrometry analysis. Genes and proteins involved in cholesterol homeostasis were detected by real-time PCR and immunoblotting, respectively. Cholesterol efflux was determined from [ 3 H]-cholesterol labeled HPEC and [ 14 C]-acetate was used as cholesterol precursor to measure cholesterol biosynthesis and esterification. We detected enhanced formation of ROS and of specific, ROS-derived oxysterols in HPEC isolated from GDM versus control pregnancies. ROS-generated oxysterols were simultaneously elevated in cord blood of GDM neonates. Liver-X receptor activation in control HPEC by synthetic agonist TO901319, 7-ketocholesterol, or 7β-hydroxycholesterol upregulated ATP-binding cassette transporters (ABC)A1 and ABCG1 expression, accompanied by increased cellular cholesterol efflux. Upregulation of ABCA1 and ABCG1 and increased cholesterol release to apoA-I and HDL 3 (78 ± 17%, 40 ± 9%, respectively) were also observed in GDM versus control HPEC. The LXR antagonist GGPP reversed ABCA1 and ABCG1 upregulation and reduced the increased cholesterol efflux in GDM HPEC. Similar total cellular cholesterol levels were detected in control and GDM HPEC, while GDM enhanced cholesterol biosynthesis along with upregulated 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) and sterol O-acyltransferase 1 (SOAT1) mRNA and protein levels. Our results suggest that in GDM cellular cholesterol homeostasis in the fetoplacental endothelium is modulated via LXR activation and helps to maintain its proper functionality. [ABSTRACT FROM AUTHOR]

Controversies persist over the most efficacious pharmacologic treatment for gestational diabetes mellitus. For purposes of accuracy in this article, the individual American College of Obstetricians and Gynecologists Practice Bulletin and American Diabetes Association Standards of Medical Care positions on each issue are quoted and then deliberated with evidence of counter claims presented in point/counterpoint. This is a review of all the relevant evidence for the most holistic picture possible. The main issues are (1) which diabetic drugs cross the placenta, (2) the quality of evidence and data source validity, (3) the rationale for the designation of glucose control as the primary outcome in gestational diabetes mellitus, and (4) which drugs (metformin, glyburide, or insulin) are most effective in improving secondary outcomes. The concept that 1 drug fits all, whether it be insulin, glyburide, or metformin, is a fallacy. Different drugs provide certain benefits but not all the benefits and not to all patients. In addition, the steps in the gestational diabetes mellitus management decision path and the current cost of the use of insulin, glyburide, or metformin are addressed. In the future, we must consider studying the potential of diabetic drugs that currently are used in nonpregnancy and incorporating the concept of precision medicine in the decision tree to maximize pregnancy outcomes. [ABSTRACT FROM AUTHOR]

Purpose This was a prospective observational cohort study that aimed to determine whether fetal sex influences the maternal and fetal outcomes of gestational diabetes mellitus (GDM). Methods In this study, 327 European primiparous women were consecutively recruited after diagnosis of GDM. AUC on the oral glucose tolerance test (OGTT), need for insulin therapy, maternal and obstetrical outcomes, and fetal fat mass (by measuring the thickness of the anterior abdominal subcutaneous tissue) were recorded and compared between the two subgroups of female and male fetuses. Findings Despite the absence of differences in multiple comparisons of the OGTT, the AUC–OGTT was significantly higher in women carrying a male fetus (22.6 [3.2] mmol/L vs 19.7 [2.8] mmol/L). The abdominal fat thickness appeared to increase with gestational age, with higher growth in male fetuses than in female fetuses. The overall risk of need for insulin therapy was significantly higher in women carrying a male fetus (odds ratio = 1.837). At delivery, birthweight was higher in males than in females only if adjusted for gestational age, similarly for placental weight, otherwise there were no significant differences between the groups in total length of gestation, rates of cesarean delivery, and Apgar scores. Implications Overall, our data propose an association between fetal sex and GDM outcomes, suggesting the hypothesis that in maternal–fetal interactions, the fetus can affect maternal glucose metabolism. [ABSTRACT FROM AUTHOR]

The effect of extracellular polymeric substances (EPS) on the meso-scale physical structure and hydraulic resistance of membrane biofilms during gravity driven membrane (GDM) filtration was investigated. Biofilms were developed on the surface of ultrafiltration membranes during dead-end filtration at ultra-low pressure (70 mbar). Biofilm EPS composition (total protein, polysaccharide and eDNA) was manipulated by growing biofilms under contrasting nutrient conditions. Nutrient conditions consisted of (i) a nutrient enriched condition with a nutrient ratio of 100:30:10 (C: N: P), (ii) a phosphorus limitation (C: N: P ratio: 100:30:0), and (iii) a nitrogen limitation (C: N: P ratio: 100:0:10). The structure of the biofilm was characterised at meso-scale using Optical Coherence Tomography (OCT). Biofilm composition was analysed with respect to total organic carbon, total cellular mass and extracellular concentrations of proteins, polysaccharides, and eDNA. 2D-confocal Raman mapping was used to characterise the functional group composition and micro-scale distribution of the biofilms EPS. Our study reveals that the composition of the EPS matrix can determine the meso-scale physical structure of membrane biofilms and in turn its hydraulic resistance. Biofilms grown under P limiting conditions were characterised by dense and homogeneous physical structures with high concentrations of polysaccharides and eDNA. Biofilm grown under nutrient enriched or N limiting conditions were characterised by heterogeneous physical structures with lower concentrations of polysaccharides and eDNA. For P limiting biofilms, 2D-confocal Raman microscopy revealed a homogeneous spatial distribution of anionic functional groups in homogeneous biofilm structures with higher polysaccharide and eDNA concentrations. This study links EPS composition, physical structure and hydraulic resistance of membrane biofilms, with practical relevance for the hydraulic performances of GDM ultrafiltration. [ABSTRACT FROM AUTHOR]

Polychlorinated Biphenyls (PCBs) and Polybrominated Diphenyl Ethers (PBDEs) are extensively present in humans and may disturb glucose metabolism during pregnancy. However, previous reports on the associations between PCBs/PBDEs levels and gestational diabetes mellitus (GDM) have been inconsistent. We performed a nested case-control study to measure the serum levels of 6 PCB and 7 PBDE congeners in early pregnancy, and to assess their associations with GDM risk and blood glucose levels. Totally, 208 serum samples (104 GDM cases and 104 controls) were included based on a prospective cohort which was carried out in Jiangsu province, China, from 2020 to 2022. The results showed that PCB-153 was the major PCB congener, whereas PBDE-47 was the predominant PBDE congener. The continuous concentrations of PCB-153, PBDE-28, and total PCB were significantly related to an increased risk of GDM, with adjusted ORs (95%CI) of 1.25 (1.04–1.50), 1.19 (1.02–1.39), and 1.37 (1.05–1.79), respectively. Potential dose-response relationships were also observed between serum levels of PCB-153 (P = 0.011), PBDE-28 (P = 0.028), total PCB (P = 0.048), and total PCB/PBDE (P = 0.010) and GDM risk. Moreover, PCB-153, PBDE-28 and total PCB levels were positively related to 1-h OGTT blood glucose (adjusted β PCB-153 : 0.14, 95%CI: 0.00–0.28; adjusted β PBDE-28 : 0.20, 95%CI: 0.08–0.32; adjusted β total PCB : 0.30, 95%CI: 0.09–0.50), whereas none of the PCBs/PBDEs were statistically related to fasting blood glucose and 2-h OGTT blood glucose (all P > 0.05). Further meta-analysis also supported the association of PCBs exposure with GDM risk. Our study provides further evidence that PCBs/PBDEs exposure may increase GDM risk during pregnancy. [Display omitted] • Serum levels of PCBs/PBDEs in early pregnancy in Jiangsu, China were investigated. • PCB-153 was the major PCBs, whereas PBDE-47 was the predominant PBDEs. • Levels of PCB-153, PBDE-28 and total PCB were positively related to GDM risk. • PCB-153, PBDE-28 and total PCB were associated with 1-h OGTT blood glucose. • Meta-Analysis also supported the association of PCBs exposure with GDM risk. [ABSTRACT FROM AUTHOR]