Relative Contribution of Gestational Weight Gain, Gestational Diabetes, and Maternal Obesity to Neonatal Fat Mass.
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ABSTRACT:
SUBMITTER: Mitanchez D
PROVIDER: S-EPMC7698189 | biostudies-literature | 2020 Nov
REPOSITORIES: biostudies-literature
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Relative Contribution of Gestational Weight Gain, Gestational Diabetes, and Maternal Obesity to Neonatal Fat Mass.
Mitanchez Delphine D Jacqueminet Sophie S Lebbah Said S Dommergues Marc M Hajage David D Ciangura Cécile C
Nutrients 20201109 11
Maternal nutritional and metabolic status influence fetal growth. This study investigated the contribution of gestational weight gain (GWG), gestational diabetes (GDM), and maternal obesity to birthweight and newborn body fat. It is a secondary analysis of a prospective study including 204 women with a pregestational body mass index (BMI) of 18.5-24.9 kg/m<sup>2</sup> and 219 women with BMI ≥ 30 kg/m<sup>2</sup>. GDM was screened in the second and third trimester and was treated by dietary inter ...[more]
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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
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:ObjectiveThe objective of this study was to determine the effectiveness of controlling maternal gestational weight gain (GWG) in the second and third trimesters on neonate body composition.MethodsTwo hundred ten healthy women with overweight (25 > BMI < 30) or obesity (BMI ≥ 30) were randomly assigned to a lifestyle intervention (LI) program focused on controlling GWG through nutrition and activity behaviors or to usual obstetrical care (UC). Infant fat and fat-free mass (FFM) at birth were measured by using air displacement plethysmography (PEA POD) and by using quantitative magnetic resonance (QMR).ResultsAt baseline, there were no between-group differences in maternal characteristics (mean [SD]): age: 33.8 (4.3) years, weight: 81.9 (13.7) kg, BMI: 30.4 (4.5), and gestational age at randomization: 14.9 (0.8) weeks. GWG was less in the LI group by 1.79 kg (P = 0.003) or 0.0501 kg/wk (P = 0.002). Compared with UC infants, LI infants had greater weight (131 ± 59 g P = 0.03), FFM (98 ± 45 g; P = 0.03) measured by PEA POD, and lean mass (105 ± 38 g; P = 0.006) measured by QMR. Fat mass and percent fat were not significantly different.ConclusionsIntervening in women with overweight and obesity through behaviors promoting healthy diet and physical activity to control GWG resulted in neonates with similar fat and greater FFM.
| S-EPMC5824435 | biostudies-literature
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:IntroductionTo date, there have only been provisional recommendations about the appropriate gestational weight gain in twin pregnancies. This study aimed to contribute evidence to this gap of knowledge.Material and methodsUsing a cohort of 10 603 twin pregnancies delivered between 2000 and 2015 in the state of Hessen, Germany, the individual and combined impact of maternal body mass index and gestational weight gain on maternal and neonatal outcomes was analyzed using uni- and multivariable logistic regression models. The analysis used newly defined population-based quartiles of gestational weight gain in women carrying twin pregnancies (Q1: <419.4 g/week [low weight gain], Q2-Q3: 419.4-692.3 g/week [optimal weight gain], Q4: >692.3 g/week [high weight gain]) and the World Health Organization body mass index classification.ResultsPre-pregnancy body mass index ≥25 kg/m2 was associated with significantly increased rates of cesarean deliveries (aOR1.2, 95% CI: 1.01-1.41) and pregnancy-induced hypertensive disorders (aOR 1.53, 95% CI: 1.11-2.1) but not with any adverse neonatal outcome. Perinatal mortality (aOR 2.23, 95% CI: 1.38-3.6), preterm birth (aOR 1.88, 95% CI: 1.58-2.25), APGAR'5 < 7 (aOR 1.61, 95% CI: 1.19-2.17) and admissions to the neonatal intensive care unit (aOR 1.6, CI: 1.38-1.85) were increased among women with low gestational weight gain. Rates of cesarean deliveries were high in both women with low (aOR 1.25, 95% CI: 1.05-1.48) and high gestational weight gain (aOR 1.17, 95% CI: 1.01-1.35). A high gestational weight gain was also associated with higher rates of hypertensive disorders in pregnancy (aOR 2.32, 95% CI: 1.79-3.02) and postpartum hemorrhage (aOR 1.72, 95%CI: 1.12-2.63). The risk of preterm birth, low Apgar scores and NICU admissions showed a converse linear relation with pre-pregnancy body mass index in women with low gestational weight gain.ConclusionsIn twin pregnancies, nonoptimal weekly maternal weight gain seems to be strongly associated with maternal and neonatal adverse outcomes. Since gestational weight gain is a modifiable risk factor, health care providers have the opportunity to counsel pregnant women with twins and target their care accordingly. Additional research to confirm the validity and generalizability of our findings in different populations is warranted.
| S-EPMC9889327 | 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: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:BackgroundNot much is known about the associations of maternal obesity and excessive gestational weight gain with body fat in infancy.ObjectiveTo examine the associations of maternal pre-pregnancy body mass index and gestational weight gain with infant subcutaneous fat.MethodsIn a population-based prospective cohort study among 845 mothers and their infants, we obtained maternal pre-pregnancy body mass index and measured maternal weight during pregnancy. At 1.5, 6 and 24months, we estimated infant total subcutaneous fat (sum of biceps, triceps, suprailiacal and subscapular skinfold thicknesses) and central-to-total subcutaneous fat ratio (sum of suprailiacal and subscapular skinfold thicknesses/total subcutaneous fat).ResultsMaternal body mass index was positively associated with higher infant body mass index from 6months onwards. Maternal body mass index was not associated with infant subcutaneous fat measures at 1.5 or 6months. A 1-standard deviation scores (SDS) higher maternal body mass index was associated with a 0.09 (95% Confidence Interval 0.01, 0.17) SDS higher infant total subcutaneous fat at 24months, but not with central-to-total subcutaneous fat ratio. No associations were present for maternal total or period-specific gestational weight gain with infant fat.ConclusionMaternal body mass index was positively associated with infant body mass index and total subcutaneous fat in late infancy. Maternal total and period-specific gestational weight gain were not associated with infant body fat mass measures.
| S-EPMC5439515 | biostudies-literature
Project description:BackgroundStudies on the relative impact of body mass index in women in childbearing age and gestational weight gain on neonatal outcomes are scarce in the Middle East.ObjectivesThe primary objective of this research was to assess the impact of maternal body mass index (BMI) and gestational weight gain (GWG) on neonatal outcomes. The effect of maternal age and folic acid supplementation before and during pregnancy was also examined.Subjects and methodsThis is a retrospective cross sectional observational study of 1000 full term deliveries of women enrolled thru the National Collaborative Perinatal Neonatal Network, in Lebanon. Maternal characteristics such as age, BMI and GWG and neonatal outcomes such as weight, height, head circumference and Apgar score were the primary studied variables in this study. Total maternal weight gain were compared to the guidelines depicted by the Institute of Medicine (IOM).ResultsThe negative outcomes of newborns such as lean body weight and macrosomia were significantly present in women who gained respectively below or above the IOM's cut-off points. Pregestational body mass index influenced significantly the infants' birth weight, in both the underweight and obese categories. Birth height, head circumference and Apgar score were not influenced by pregestational body mass index or gestational weight gain. No significant associations were found between maternal age and pregestational body mass index and gestational weight gain.ConclusionStudies evaluating the impact of weight before and during pregnancy on neonatal outcomes and anthropometrics measurements are lacking in the Middle East. Our results highlight the importance of nutritional counseling in order to shed the extra weights before conceiving and monitor weight gain to avoid the negative impact on feto-maternal health.
| S-EPMC5513447 | biostudies-literature
Project description:Fatty acids (FAs) are fundamental for a foetus's growth, serving as an energy source, structural constituents of cellular membranes and precursors of bioactive molecules, as well as being essential for cell signalling. Long-chain polyunsaturated FAs (LC-PUFAs) are pivotal in brain and visual development. It is of interest to investigate whether and how specific pregnancy conditions, which alter fatty acid metabolism (excessive pre-pregnancy body mass index (BMI) or gestational weight gain (GWG)), affect lipid supply to the foetus. For this purpose, we evaluated the erythrocyte FAs of mothers and offspring (cord-blood) at birth, in relation to pre-pregnancy BMI and GWG. A total of 435 mothers and their offspring (237 males, 51%) were included in the study. Distribution of linoleic acid (LA) and α-linolenic acid (ALA), and their metabolites, arachidonic acid, dihomogamma linoleic (DGLA) and ecosapentanoic acid, was significantly different in maternal and foetal erythrocytes. Pre-pregnancy BMI was significantly associated with maternal percentage of MUFAs (Coeff: -0.112; p = 0.021), LA (Coeff: -0.033; p = 0.044) and DHA (Coeff. = 0.055; p = 0.0016); inadequate GWG with DPA (Coeff: 0.637; p = 0.001); excessive GWG with docosaexahenoic acid (DHA) (Coeff. = -0.714; p = 0.004). Moreover, pre-pregnancy BMI was associated with foetus percentage of PUFAs (Coeff: -0.172; p = 0.009), omega 6 (Coeff: -0.098; p = 0.015) and DHA (Coeff: -0.0285; p = 0.036), even after adjusting for maternal lipids. Our findings show that maternal GWG affects maternal but not foetal lipid profile, differently from pre-pregnancy BMI, which influences both.
| S-EPMC4924209 | biostudies-literature