Obesity and diabetes genetic variants associated with gestational weight gain.
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ABSTRACT: Objective
We sought to determine whether genetic variants associated with diabetes and obesity predict gestational weight gain.Study design
A total of 960 participants in the Pregnancy, Infection, and Nutrition cohorts were genotyped for 27 single-nucleotide polymorphisms (SNPs) associated with diabetes and obesity.Results
Among Caucasian and African American women (n = 960), KCNQ1 risk allele carriage was directly associated with weight gain (P < .01). In Bayesian hierarchical models among Caucasian women (n = 628), we found posterior odds ratios >3 for inclusion of TCF2 and THADA SNPs in our models. Among African American women (n = 332), we found associations between risk allele carriage and weight gain for the THADA and INSIG2 SNPs. In Bayesian variable selection models, we found an interaction between the TSPAN8 risk allele and pregravid obesity, with lower weight gain among obese risk allele carriers.Conclusion
We found evidence that diabetes and obesity risk alleles interact with maternal pregravid body mass index to predict gestational weight gain.
SUBMITTER: Stuebe AM
PROVIDER: S-EPMC3222335 | biostudies-literature | 2010 Sep
REPOSITORIES: biostudies-literature
Publications
Obesity and diabetes genetic variants associated with gestational weight gain.
Stuebe Alison M AM Lyon Helen H Herring Amy H AH Ghosh Joyee J Wise Alison A North Kari E KE Siega-Riz Anna Maria AM
American journal of obstetrics and gynecology 20100901 3
<h4>Objective</h4>We sought to determine whether genetic variants associated with diabetes and obesity predict gestational weight gain.<h4>Study design</h4>A total of 960 participants in the Pregnancy, Infection, and Nutrition cohorts were genotyped for 27 single-nucleotide polymorphisms (SNPs) associated with diabetes and obesity.<h4>Results</h4>Among Caucasian and African American women (n = 960), KCNQ1 risk allele carriage was directly associated with weight gain (P < .01). In Bayesian hierar ...[more]
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Project description:Introduction:Pre-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 methods:Women 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. Results:The 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). Conclusion:The 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:Background:Our objective was to examine the associations of parental body mass index (BMI) and maternal gestational weight gain with childhood-onset type 1 diabetes. Comparing the associations of maternal and paternal BMI with type 1 diabetes in the offspring will provide further insight into the role of unmeasured confounding by characteristics linked to BMI in both parents. Methods:We studied 132 331 children participating in the Norwegian Mother and Child Cohort Study (MoBa) and the Danish National Birth Cohort (DNBC) who were born between February 1998 and July 2009. Exposures of interest included parental BMI and maternal gestational weight gain obtained by maternal report. We used Cox-proportional hazards regression to examine the risk of type 1 diabetes (n=499 cases), which was ascertained by national childhood diabetes registers. Results:The incidence of type 1 diabetes was 32.7 per 100 000 person-years in MoBa and 28.5 per 100 000 person-years in DNBC. Both maternal pre-pregnancy obesity, adjusted hazard ratio (HR) 1.41 [95% confidence interval (CI): 1.06, 1.89] and paternal obesity, adjusted HR 1.51 (95% CI: 1.11, 2.04), were associated with childhood-onset type 1 diabetes. The associations were similar after mutual adjustment. In contrast, maternal total gestational weight gain was not associated with childhood-onset type 1 diabetes, adjusted HR 1.00 (95% CI: 0.99, 1.02) per kilogram increase. Conclusions:Our study suggests that the association between maternal obesity and childhood-onset type 1 diabetes is not likely explained by intrauterine mechanisms, but possibly rather by unknown environmental factors influencing BMI in the family.
| S-EPMC5913633 | biostudies-literature
Project description: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/m2 and 219 women with BMI ? 30 kg/m2. GDM was screened in the second and third trimester and was treated by dietary intervention, and insulin if required. Maternal obesity had the greatest effect on skinfolds (+1.4 mm) and cord leptin (+3.5 ng/mL), but no effect on birthweight. GWG was associated with increased birthweight and skinfolds thickness, independently from GDM and maternal obesity. There was an interaction between third trimester weight gain and GDM on birthweight and cord leptin, but not with maternal obesity. On average, +1 kg in third trimester was associated with +13 g in birthweight and with +0.64 ng/mL in cord leptin, and a further 32 g and 0.89 ng/mL increase in diabetic mothers, respectively. Maternal obesity is the main contributor to neonatal body fat. There is an independent association between third trimester weight gain, birthweight, and neonatal body fat, enhanced by GDM despite intensive treatment.
| S-EPMC7698189 | biostudies-literature
Project description:Gestational weight gain (GWG) is associated with a range of health outcomes, but little is known about the factors that influence it.The objective was to test the hypothesis that maternal and fetal genetic variants that are reliably associated with adiposity are associated with GWG.We examined the association of a risk allele score by using 4 adiposity-related single nucleotide polymorphisms (SNPs; rs9939609 in FTO, rs17782313 near MC4R, rs6548238 near TMEM18, and rs10938397 near GNPDA2) with GWG in a pregnancy cohort in which women had detailed repeated assessment of GWG (median number of weight measurements: 10; interquartile range: 8, 11). The numbers included in our analyses varied between 2324 and 7563 for different variant-outcome analyses. A linear spline random-effects model was used to model weight change with gestational age and to relate genetic variants to this. This modeling confirmed 3 distinct periods of GWG: 0-18, 19-28, and ?29 wk of gestation.Maternal risk allele score and SNPs in FTO, MC4R, and TMEM18 were positively associated with prepregnancy weight. Maternal allele score was inversely associated with GWG in the first 18 wk of pregnancy (-14.46 g/wk per allele; 95% CI: -24.75, -4.17 g/wk per allele) but was not associated with other periods of GWG. Offspring allele score and maternal and offspring individual SNPs were not associated with GWG in any period or with birth weight or postnatal weight retention.Our findings suggest that neither maternal nor fetal adiposity-related genetic variants are associated with greater GWG. The inverse association of maternal allele score with GWG in the first 18 wk requires replication.
| S-EPMC3127507 | biostudies-literature
Project description:OBJECTIVE:We examined the association between gestational weight gain (GWG) and offspring obesity at age 36 months. METHODS:Mother-infant dyads (n?=?609) were followed from a first study visit (mean [standard deviation]: 18.8 [2.7] weeks gestation) to 36 months postpartum. Total GWG over the entire pregnancy was defined as excessive or non-excessive according to the 2009 Institute of Medicine guidelines. Four mutually exclusive categories of excessive or non-excessive GWG across early (conception to first study visit) and late (first study visit to delivery) pregnancy defined GWG pattern. Body mass index (BMI) z-scores ?95th percentile of the 2000 Centers for Disease Control (CDC) references defined offspring obesity at 36 months. Multivariable log-binomial models adjusted for pre-pregnancy BMI and breastfeeding were used to estimate the association between GWG and childhood obesity risk. RESULTS:Nearly half of the women had total excessive GWG. Of these, 46% gained excessively during both early and late pregnancy while 22% gained excessively early and non-excessively late, and the remaining 32% gained non-excess weight early and excessively later. Thirteen per cent of all children were obese at 36 months. Excessive total GWG was associated with more than twice the risk of child obesity (adjusted risk ratio [95% confidence interval]: 2.20 [1.35, 3.61]) compared with overall non-excessive GWG. Compared with a pattern of non-excessive GWG in both early and late pregnancy, excessive GWG in both periods was associated with an increased risk of obesity (2.39 [1.13, 5.08]). CONCLUSIONS:Excessive GWG is a potentially modifiable factor that may influence obesity development in early childhood.
| S-EPMC4379119 | biostudies-literature
Project description:ObjectiveThe purpose of this study was to evaluate the independent contribution of maternal obesity and gestational weight gain (GWG) in excess of the Institute of Medicine's guidelines on levels of maternal serum inflammatory and metabolic measures.Study designBanked maternal serum samples from 120 subjects with documented prepregnancy or first trimester body mass index (BMI) were utilized for analyte analyses. Validated, BMI-specific formulas were utilized to categorize GWG as either insufficient, at goal or excess based on the Institute of Medicine guidelines with gestational age adjustments. Serum was analyzed for known inflammatory or metabolic pathway intermediates using the Luminex xMap system with the MILLIPLEX Human Metabolic Hormone Magnetic Bead Panel. Measured analytes included interleukin-6, monocyte chemoattractant protein-1, and tumor necrosis factor-α and metabolic markers amylin, c-peptide, ghrelin, gastric inhibitory polypeptide, glucagon-like peptide-1, glucagon, insulin, leptin, pancreatic polypeptide, and peptide YY. Kruskal-Wallis ANOVA and Pearson's correlation coefficients were calculated for each marker.ResultsC-peptide, insulin, and leptin all varied significantly with both obesity and GWG while glucagon-like peptide-1 varied by BMI but not GWG. These analytes covaried with other metabolic analytes, but not with inflammatory analytes.ConclusionMaternal metabolic biomarkers at delivery vary significantly with both obesity and GWG. Taken together, these findings suggest that GWG (with and without comorbid obesity) is an important mediator of measurable metabolites in pregnancy but is not necessarily accompanied by inflammatory measures in serum. These findings are consistent with GWG being an independent risk factor for metabolic disturbances during pregnancy.
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Project description:Excessive pre-pregnancy weight is a known risk factor of pregnancy complications. The purpose of this analysis was to assess the relationship between several categories of maternal weight and the risk of developing hypertension and diabetes in pregnancy, and the relationship of these complications with the results of the newborn. It was carried out in a common cohort of pregnant women and taking into account the influence of disturbing factors. Our analysis was conducted in a prospective cohort of 912 Polish pregnant women, recruited during 2015-2016. We evaluated the women who subsequently developed diabetes with dietary modification (GDM-1) (n = 125) and with insulin therapy (GDM-2) (n = 21), as well as the women who developed gestational hypertension (GH) (n = 113) and preeclampsia (PE) (n = 24), compared to the healthy controls. Odds ratios of the complications (and confidence intervals (95%)) were calculated in the multivariate logistic regression. In the cohort, 10.8% of the women had pre-pregnancy obesity (body mass index (BMI) ? 30 kg/m2), and 36.8% had gestational weight gain (GWG) above the range of the Institute of Medicine recommendation. After correction for excessive GWG and other confounders, pre-pregnancy obesity (vs. normal BMI) was associated with a higher odds ratio of GH (AOR = 4.94; p < 0.001), PE (AOR = 8.61; p < 0.001), GDM-1 (AOR = 2.99; p < 0.001), and GDM-2 (AOR = 11.88; p <0.001). The threshold risk of development of GDM-2 occurred at lower BMI values (26.9 kg/m2), compared to GDM-1 (29.1 kg/m2). The threshold point for GH was 24.3 kg/m2, and for PE 23.1 kg/m2. For GWG above the range (vs. GWG in the range), the adjusted odds ratios of GH, PE, GDM-1, and GDM-2 were AOR = 1.71 (p = 0.045), AOR = 1.14 (p = 0.803), AOR = 0.74 (p = 0.245), and AOR = 0.76 (p = 0.672), respectively. The effect of maternal edema on all the results was negligible. In our cohort, hypertension and diabetes were associated with incorrect birth weight and gestational age at delivery. Conclusions: This study highlights the importance and influence of excessive pre-pregnancy maternal weight on the risk of pregnancy complications such as diabetes and hypertension which can impact fetal outcomes.
| S-EPMC7355601 | 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:Growing evidence links perceived stress-a potentially modifiable psychosocial risk factor-with health behaviors and obesity. Yet little is known about the relationship between stress during pregnancy and gestational weight gain, particularly among women with pregnancy complications. We conducted a cross-sectional analysis to examine associations between psychosocial stress during pregnancy and gestational weight gain among women with gestational diabetes. We used baseline data from the Gestational Diabetes's Effects on Moms (GEM) study: 1,353 women with gestational diabetes who delivered a term singleton within Kaiser Permanente Northern California were included. Perceived stress near the time of gestational diabetes diagnosis was measured using the validated Perceived Stress Scale (PSS10). Gestational weight gain was categorized according to the 2009 Institute of Medicine recommendations. Binomial regression analyses adjusted for gestational age and maternal age at the time of gestational diabetes diagnosis, and race/ethnicity and estimated rate ratios (RR) and their 95% confidence interval (CI). Among women with a normal pregravid Body Mass Index (BMI 18.5-24.9 kg/m2), there was a significant association between high (Q4) PSS score and risk of both exceeding and gaining below the Institute of Medicine recommendations compared to those with lower stress (Q1) [adjusted RR = 2.16 95% CI 1.45-3.21; RR = 1.39 95% CI 1.01-1.91, respectively.] Among women with pregravid overweight/obesity (BMI≥25 kg/m2), there was no association. Although the temporal relationship could not be established from this study, there may be a complex interplay between psychosocial stress and gestational weight gain among women with gestational diabetes. Further studies examining stress earlier in pregnancy, risk of developing gestational diabetes and excess/inadequate gestational weight gain are warranted to clarify these complex relationships.
| S-EPMC5369756 | biostudies-literature
Project description:To estimate the prevalence of gestational weight gain adequacy according to the 2009 Institute of Medicine recommendations and examine demographic, behavioral, psychosocial, and medical characteristics associated with inadequate and excessive gain stratified by prepregnancy body mass index (BMI) category.We used cross-sectional, population-based data on women delivering full-term (37 weeks of gestation or greater), singleton neonates in 28 states who participated in the 2010 or 2011 Pregnancy Risk Assessment Monitoring System. We estimated adjusted odds ratios (ORs) and 95% confidence intervals (CIs) for inadequate and excessive compared with adequate gain, stratified by prepregnancy BMI.Overall, 20.9%, 32.0%, and 47.2% of women gained inadequate, adequate, and excessive gestational weight, respectively. Prepregnancy BMI was strongly associated with weight gain outside recommendations. Compared with normal-weight women (prevalence 51.8%), underweight women (4.2%) had decreased odds of excessive gain (adjusted OR 0.50, CI 0.40-0.61), whereas overweight and obese class I, II, and III (23.6%, 11.7%, 5.4%, and 3.5%, respectively) women had increased odds of excessive gain (adjusted OR range 2.07, CI 1.63-2.62 to adjusted OR 2.99, CI 2.63-3.40). Underweight and obese class II and III women had increased odds of inadequate gain (adjusted OR 1.25, CI 1.01-1.55 to 1.86, CI 1.45-2.36). Most characteristics associated with weight gain adequacy were demographic such as racial or ethnic minority status and education and varied by prepregnancy BMI. Notably, one behavioral characteristic-smoking cessation-was associated with excessive gain among normal-weight and obese women.Most women gained weight outside recommendations. Understanding characteristics associated with inadequate or excessive weight gain may identify potentially at-risk women and inform much-needed interventions.
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