Increased epigenetic alterations at the promoters of transcriptional regulators following inadequate maternal gestational weight gain.
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ABSTRACT:
SUBMITTER: Kawai T
PROVIDER: S-EPMC4586460 | biostudies-literature | 2015
REPOSITORIES: biostudies-literature
Publications
Increased epigenetic alterations at the promoters of transcriptional regulators following inadequate maternal gestational weight gain.
Kawai Tomoko T Yamada Takahiro T Abe Kosei K Okamura Kohji K Kamura Hiromi H Akaishi Rina R Minakami Hisanori H Nakabayashi Kazuhiko K Hata Kenichiro K
Scientific reports 20150929
Epigenetic modifications are thought to serve as a memory of exposure to in utero environments. However, few human studies have investigated the associations between maternal nutritional conditions during pregnancy and epigenetic alterations in offspring. In this study, we report genome-wide methylation profiles for 33 postpartum placentas from pregnancies of normal and foetal growth restriction with various extents of maternal gestational weight gain. Epigenetic alterations accumulate in the pl ...[more]
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Project description:The concept that fetal environment correlates with health later on has been defined as developmental origins of health and disease (DOHaD), in which epigenetic modifications are considered to serve as a memory of exposure to in utero environments. Although many animal studies have demonstrated direct associations of maternal nutritional conditions during pregnancy with epigenetic alterations in the offspring, such evidence from human studies has been very limited. To gain more insight into the effects of in utero environments on the human placental epigenome, we obtained genome-wide methylation profiles for 34 postpartum placentas from pregnancies of normal and fetal growth restriction cases with various extents of maternal gestational weight gain (GWG). Whereas we initially failed to identify specific loci whose methylation is commonly altered across all subjects in each of subgroups categorized by the extent of GWG and baby’s birth weight, the application of Smirnov-Grubbs' outlier test to the same dataset revealed the accumulation of epigenetic alterations in the placentas under the adverse in utero environments. This methodology is potentially applicable to various epigenome studies for human populations. Further annotations of the genomic and functional features of loci with altered DNA methylation demonstrated that environmentally induced hyper-methylation is significantly frequently occurred at the promoter region of transcriptional regulator genes including polycomb-targets and zinc-finger genes. Aberrant epigenetic modifications at such developmental regulator loci, if occurred in fetuses in a similar manner as observed in the placentas examined in this study, would elevate the risk of developing various diseases including metabolic and mental disorders in the later life.
2015-09-30 | GSE62733 | GEO
Project description:The aims were to investigate the association of maternal pre-pregnancy body mass index (BMI) and gestational weight gain (GWG) with breastfeeding (BF) duration and BF pattern at 3 months of age.This was a prospective cohort study of 4231 children who were enrolled at birth and were followed-up at 3, 12, 24 and 48 months of age to gather information on maternal and offspring characteristics including BF patterns and BF duration. Maternal pre-pregnancy BMI was categorized according to the WHO classification and GWG according to the 2009 Institute of Medicine recommendations. Cox's proportional hazards model was used to assess whether pre-pregnancy BMI and GWG were associated with BF and exclusive breastfeeding (EBF) duration. Predicted probabilities of BF patterns at 3 months were estimated by multinomial logistic regression.Information on BF was available to 4011 infants. The total BF and EBF median durations were 7.0 months and 1.5 months, respectively. There were no differences in duration of any BF or EBF according to pre-pregnancy BMI or GWG categories. There was an increased predicted probability for weaning before the age of 3 months among infants from obese women, compared with those from mothers with normal pre-pregnancy BMI, with margins adjusted predictions of 0.36 (95% confidence interval (CI) 0.31-0.41) and 0.23 (95% CI 0.21-0.25), respectively.Infants from pre-pregnancy overweight/obese mothers presented higher probability of early weaning compared with infants from normal-weight mothers. Obese/overweight pregnant women need supplementary guidance about BF benefits to infant health during prenatal and postnatal care.
| S-EPMC4827014 | biostudies-other
Project description:BackgroundMaternal metabolic abnormalities have been related to offspring obesity especially during childhood.ObjectivesWe analyzed whether the gestational diabetes mellitus (GDM)-associated melatonin receptor 1B (MTNR1B) genotype of mothers modified the relation between maternal gestational weight gain and childhood obesity.MethodsA total of 1114 Chinese mother-child pairs (mothers with or without prior GDM) were included. Mothers' MTNR1B rs10830962 genotype and gestational weight gain were assessed. Indicators of childhood obesity included BMI-for-age z-score, weight-for-age z-score, waist circumference, and body fat. Childhood overweight and obesity were also analyzed.ResultsWe found that the maternal MTNR1B genotype significantly interacted with gestational weight gain on indicators of offspring's obesity (all P for interaction < 0.05). After multivariable adjustment, BMI-for-age z-scores associated with 1-kg gestational weight gain were 0.009 (SE 0.018), 0.026 (SE 0.010), and 0.061 (SE 0.010) in children with the maternal MTNR1B genotype CC, CG, and GG, respectively (P-interaction = 0.012). Similar interactions were observed for weight-for-age z-score, waist circumference, and body fat (P-interaction = 0.001, 0.003, and 0.012, respectively). The associations remained consistently significant in women with and without GDM. We also found significant interactions between the maternal MTNR1B genotype and gestational weight gain on the offspring's childhood overweight and obesity (P-interaction = 0.005 and 0.026, respectively).ConclusionsThe maternal MTNR1B genotype might interact with gestational weight gain on offspring's obesity risk during childhood.
| S-EPMC6997086 | biostudies-literature
Project description:BackgroundClinical recommendations to limit gestational weight gain (GWG) imply high GWG is causally related to adverse outcomes in mother or offspring, but GWG is the sum of several inter-related complex phenotypes (maternal fat deposition and vascular expansion, placenta, amniotic fluid and fetal growth). Understanding the genetic contribution to GWG could help clarify the potential effect of its different components on maternal and offspring health. Here we explore the genetic contribution to total, early and late GWG.Participants and methodsA genome-wide association study was used to identify maternal and fetal variants contributing to GWG in up to 10 543 mothers and 16 317 offspring of European origin, with replication in 10 660 mothers and 7561 offspring. Additional analyses determined the proportion of variability in GWG from maternal and fetal common genetic variants and the overlap of established genome-wide significant variants for phenotypes relevant to GWG (for example, maternal body mass index (BMI) and glucose, birth weight).ResultsApproximately 20% of the variability in GWG was tagged by common maternal genetic variants, and the fetal genome made a surprisingly minor contribution to explain variation in GWG. Variants near the pregnancy-specific beta-1 glycoprotein 5 (PSG5) gene reached genome-wide significance (P=1.71 × 10-8) for total GWG in the offspring genome, but did not replicate. Some established variants associated with increased BMI, fasting glucose and type 2 diabetes were associated with lower early, and higher later GWG. Maternal variants related to higher systolic blood pressure were related to lower late GWG. Established maternal and fetal birth weight variants were largely unrelated to GWG.ConclusionsWe found a modest contribution of maternal common variants to GWG and some overlap of maternal BMI, glucose and type 2 diabetes variants with GWG. These findings suggest that associations between GWG and later offspring/maternal outcomes may be due to the relationship of maternal BMI and diabetes with GWG.
| S-EPMC5784805 | biostudies-literature
Project description:Data on the association of maternal gestational weight gain (GWG) and gestational diabetes mellitus (GDM) with childhood asthma are limited and inconsistent. We aimed to investigate these associations in a U.S. pre-birth cohort. Analyses included 16,351 mother-child pairs enrolled in the Massachusetts General Hospital Maternal-Child Cohort (1998-2010). Data were obtained by linking electronic health records for prenatal visits/delivery to determine BMI, GWG, and GDM (National Diabetes Data Group criteria) and to determine asthma incidence and allergies (atopic dermatitis or allergic rhinitis) for children. The associations of prenatal exposures with asthma were evaluated using logistic regression adjusted for maternal characteristics. A total of 2306 children (14%) developed asthma by age 5 years. Overall, no association was found between GWG and asthma. GDM was positively associated with offspring asthma (OR 1.46, 95% CI 1.14-1.88). Associations between GDM and asthma were observed only among mothers with early pregnancy BMI between 20 and 24.9 kg/m2 (OR 2.31, CI 1.46-3.65, p-interaction 0.02). We report novel findings on the impact of prenatal exposures on asthma, including increased risk among mothers with GDM, particularly those with a normal BMI. These findings support the strengthening of interventions targeted toward a healthier pregnancy, which may also be helpful for childhood asthma prevention.
| S-EPMC9741125 | biostudies-literature
Project description:BackgroundMaternal obesity may affect offspring asthma and atopic disease risk by altering fetal immune system development. However, few studies evaluate gestational weight gain (GWG).ObjectiveTo evaluate relationships between maternal body mass index (BMI), GWG, and persistent wheeze, eczema, allergy, and asthma risk in offspring through middle childhood.MethodsA total of 5939 children from Upstate KIDS, a population-based longitudinal cohort of children born in upstate New York (2008-2019) were included in the analysis. Persistent wheeze or asthma, eczema, and allergy were maternally reported at multiple study time points throughout early and middle childhood. Poisson regression models with robust SEs were used to estimate adjusted risk ratios (aRRs) and 95% confidence intervals (CIs) for offspring atopic outcomes by maternal prepregnancy BMI and GWG.ResultsPrepregnancy BMI was associated with increased risk of persistent wheeze by 3 years of age even after adjustments for maternal atopy (class I obesity: aRR, 1.58; 95% CI, 1.13-2.20; class II or III obesity: aRR, 1.69; 95% CI, 1.22-2.35). Associations with reported asthma in middle childhood did not reach statistical significance. Furthermore, no associations were found between prepregnancy BMI and atopic outcomes in either early or middle childhood. GWG was not associated with higher risk of early childhood persistent wheeze or middle childhood asthma.ConclusionMaternal prepregnancy BMI was associated with increased risk of offspring wheeze, whereas excessive GWG was generally not associated with childhood asthma or atopy.
| S-EPMC9329274 | biostudies-literature
Project description:The authors tested whether the relation between gestational weight gain (GWG) and 5 adverse pregnancy outcomes (small-for-gestational-age (SGA) birth, large-for-gestational-age (LGA) birth, spontaneous preterm birth, indicated preterm birth, and unplanned cesarean delivery) differed according to maternal race/ethnicity, smoking, parity, age, and/or height. They also evaluated whether GWG guidelines should be modified for special populations by studying GWG and risk of at least 1 adverse outcome within different subgroups. Data came from a cohort of 23,362 normal-weight mothers who delivered singletons at Magee-Womens Hospital in Pittsburgh, Pennsylvania (2003-2008). Adequacy of GWG was defined as observed GWG divided by recommended GWG. The synergy analysis found that the combination of smoking, black race/ethnicity, primiparity, or short height with poor GWG was associated with an excess risk of SGA birth, while high GWG combined with each of these characteristics diminished risk of LGA birth in comparison with the same GWG among the women's counterparts. Nevertheless, there were no significant or meaningful differences in the risk of at least 1 adverse outcome between the GWG recommended by the Institute of Medicine in 2009 and the GWG that minimized risk of the composite outcome. These findings do not support the tailoring of GWG guidelines on the basis of a mother's smoking status, race/ethnicity, parity, age, or height among normal-weight women.
| S-EPMC3167680 | biostudies-literature
Project description:Weight gain in pregnancy is an essential physiologic adaptation that supports growth and development of a fetus and is distributed among lean mass that includes total body water and fat mass gains. Although gestational weight gain provides a source of energy for the mother and fetus, excess gestational weight gain may underlie reported associations between parity and future metabolic disorders and is linked to postpartum weight retention and insulin resistance. Although weight gain often is proposed as a modifiable variable to mitigate adverse maternal and offspring health outcomes, our knowledge of specific maternal body composition changes with weight gain and the potential metabolic consequences is limited. Furthermore, although gestational weight gain alters maternal body composition, the impact of excess weight gain on fat and lean mass is not well-studied. Understanding the accrual of fat and lean body mass may improve our understanding of the role of excessive gestational weight gain and metabolic dysfunction.The purpose of our study was to quantify the relationship between gestational weight gain and maternal fat and lean body mass accrual and to compare fat and lean body mass accrual according to the 2009 Institute of Medicine Guidelines for Gestational Weight Gain in Pregnancy adherence. We hypothesized that exceeding current weight gain guidelines would be associated with greater fat, compared with lean body, mass accrual.This is a secondary analysis of a randomized controlled trial of 49 overweight/obese women; all 49 are included in this secondary analysis. Maternal weight and body composition were collected in early (13 0/6 to 16 6/7 weeks gestation) and late (34 0/7 to 36 6/7 weeks gestation) pregnancy with the use of air densitometry. Correlations were drawn between gestational weight gain and change in fat and lean body mass. We compared change in fat and lean body mass by adherence to the 2009 Institute of Medicine Guidelines for Gestational Weight Gain in Pregnancy. Nonparametric tests and chi-square analyses were performed; a probability value of <.05 was significant.Early pregnancy body mass index was 30.3 kg/m(2) (interquartile range [IQR], 28.5-35.2 kg/m(2)); women gained 9.0 kg (IQR, 5.3-13.2 kg). Overweight and obese women were equally likely to gain excess weight (48% vs 35%; P = .6). Weight gain correlated strongly with fat mass change (r = 0.87; P < .001); women with excess vs adequate vs inadequate weight gain had greater fat mass change overall (5.2 [IQR, 4.2-8.1] vs 0.2 [IQR, -0.4-2.2] vs -2.7 [IQR, -5.2- -0.7] kg, respectively; P < .001) and in all pairwise comparisons. Weight gain also correlated with lean body mass change (r = 0.52; P = .001), but women with excess vs adequate weight gain had similar lean body mass change (8.4 [IQR, 7.2-10.1] vs 7.8 [IQR, 6.0-8.7] kg; P = .1).Excess gestational weight gain is associated primarily with maternal fat, but not with lean body mass accrual. Our results may help explain the reason that excess gestational weight gain or fat mass accrual is associated with long-term obesity, metabolic dysfunction, and cardiovascular disease risk.
| S-EPMC4884531 | biostudies-literature
Project description:ImportanceInformation on the association between maternal prepregnancy body weight, gestational weight change, and childhood allergies is not consistent. Little is known on whether there is a combined association with comprehensive childhood allergies.ObjectiveTo examine the association of maternal prepregnancy body mass index and gestational weight gain (GWG) with the risk of childhood allergic diseases including asthma and/or wheezing, allergic rhinitis, eczema, and food and/or drug allergy.Design, setting, and participantsThis cross-sectional study was conducted from April 12 to June 1, 2019, using the Shanghai Children Allergy Study (SCAS), a large, population-based survey. A multistage and multistrata sampling approach was applied to conduct the survey in 13 districts across Shanghai, China, with an enrollment of 15 145 mother-child pairs.ExposuresReported maternal weight before pregnancy and at the time of delivery were requested in the survey; GWG was examined in absolute terms and with reference to the Institute of Medicine guideline.Main outcomes and measuresThe ascertainment of allergic diseases was based on the International Study of Asthma and Allergies in Childhood questionnaire.ResultsAmong 15 145 children aged 3 to 14 years (7911 [52.2%] boys) within the SCAS, 8877 children (58.6%) were screened for allergic diseases. Multivariable log-binomial regression models suggested that excessive GWG was associated with risks of 19% for asthma/wheezing, 11% for allergic rhinitis, and 10% for eczema in the children. Gestational weight gain extremely above the Institute of Medicine guideline in women who were overweight/obese before pregnancy was associated with the highest risk of childhood asthma/wheezing (adjusted prevalence ratio, 1.42; 95% CI, 1.16-1.74; P = .001), allergic rhinitis (adjusted prevalence ratio, 1.32; 95% CI, 1.12-1.56; P = .001), and eczema (adjusted prevalence ratio, 1.24; 95% CI, 1.08-1.41; P = .002). Gestational weight gain below the Institute of Medicine guideline was associated with an attenuated risk of 13% for childhood asthma/wheezing, 11% for allergic rhinitis, 14% for eczema, and 15% food/drug allergy when mothers were of prepregnancy normal weight; similar associations were observed in underweight mothers, but there was no association in overweight mothers. Generally, the associations were similar in the stratified analysis according to children's age group. Moreover, the results were similar in the allergen test subgroup.Conclusions and relevanceThe findings of this study suggest that excessive GWG may be a risk factor for childhood allergic diseases. Further studies on the long-term effects of the intrauterine environment on children's health may take maternal weight management during pregnancy into consideration since GWG could be a controllable and modifiable risk factor.
| S-EPMC7489810 | biostudies-literature
Project description:IntroductionPre-pregnancy obesity, gestational diabetes mellitus (GDM), and gestational weight gain (GWG) are associated with each other. This is the first study to investigate whether genetic variants were associated with having GDM, and whether genetic variants-related GDM were associated with adiposity including pre-pregnancy obesity and excessive GWG in Turkish women.Patients and methodsWomen with GDM (n = 160) and without GDM (n = 145) were included in case-controlled study. Genotyping of the HNF1A gene (p.I27L rs1169288, p.98V rs1800574, p.S487N rs2464196), the VDR gene (p.BsmI rs1544410, p.ApaI rs7975232, p.TaqI rs731236, p.FokI rs2228570), and FTO gene (rs9939609) SNPs were performed by using RT-PCR.ResultsThe FTO AA genotype was associated with an increased risk of having GDM (AA vs. AT + TT, 24.4% vs. 12.4%, OR = 2.27, 95% CI [1.23-4.19], p = 0.007). The HNF1A p.I27L GT/TT genotype was associated with increased GDM risk (GT + TT vs. GG-wild, 79.4% vs. 65.5%, OR = 2.02, 95% CI 1.21-3.38], p = 0.007). However, all VDR gene SNPs and the HNF1A p.A98V, p.S487N were not associated with having GDM (p > 0.05). The FTO AA genotype was associated with an increased risk for pre-pregnancy overweight/obesity (OR = 1.43, 95% CI [1.25-3.4], p = 0.035), but not associated with excessive GWG after adjusting for pre-pregnancy weight (p > 0.05). Pre-pregnancy weight, weight at delivery, and GWG did not differ in both VDR and HNF1A gene carriers (p > 0.05). HOMA-IR and HbA1c were increased in both p.I27L TT and FTO AA genotype carriers (p < 0.05).ConclusionThe adiposity-related gene FTO is associated with GDM by the effect of FTO on pre-pregnancy obesity. The diabetes-related p.I27L gene is associated with GDM by increasing insulin resistance.
| S-EPMC6518700 | biostudies-literature