FTO genotype, vitamin D status, and weight gain during childhood.
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ABSTRACT:
SUBMITTER: Lourenco BH
PROVIDER: S-EPMC3900536 | biostudies-literature |
REPOSITORIES: biostudies-literature
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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:BackgroundLow concentration of 25-hydroxyvitamin D during pregnancy may be associated with offspring autoimmune disorders. Little is known about environmental triggers except gluten for celiac disease, a common immune-mediated disorder where seasonality of birth has been reported as a risk factor. We therefore aimed to test whether low maternal and neonatal 25-hydroxyvitamin D predicted higher risk of childhood celiac disease.Methods and findingsIn this Norwegian nationwide pregnancy cohort (n = 113,053) and nested case-control study, we analyzed 25-hydroxyvitamin D in maternal blood from mid-pregnancy, postpartum and cord plasma of 416 children who developed celiac disease and 570 randomly selected controls. Mothers and children were genotyped for established celiac disease and vitamin D metabolism variants. We used mixed linear regression models and logistic regression to study associations. There was no significant difference in average 25-hydroxyvitamin D between cases and controls (63.1 and 62.1 nmol/l, respectively, p = 0.28), and no significant linear trend (adjusted odds ratio per 10 nM increase 1.05, 95% CI: 0.93-1.17). Results were similar when analyzing the mid-pregnancy, postpartum or cord plasma separately. Genetic variants for vitamin D deficiency were not associated with celiac disease (odds ratio per risk allele of the child, 1.00; 95% CI, 0.90 to 1.10, odds ratio per risk allele of the mother 0.94; 95% CI 0.85 to 1.04). Vitamin D intake in pregnancy or by the child in early life did not predict later celiac disease. Adjustment for established genetic risk markers for celiac disease gave similar results.ConclusionsWe found no support for the hypothesis that maternal or neonatal vitamin D status is related to the risk of childhood celiac disease.
| S-EPMC5501391 | biostudies-literature
Project description:Polymorphisms in the Fat Mass and Obesity Associated (FTO) gene are robustly associated with overweight and obesity among children, although the underlying mechanisms are poorly understood. We tested if appetitive traits partially mediated the association between FTO genotype and increased BMI among a sample of US preadolescents. Data were from 178 unrelated 9-10 year olds who participated in an experimental study between 2013 and 2015. Children's DNA was isolated from buccal swabs, and the rs9939609 SNP in the FTO gene was genotyped. Children's age- and sex-adjusted BMI z-scores were computed using height and weight measured at the laboratory. Parents completed the Child Eating Behavior Questionnaire that includes three validated scales of habitual appetitive traits related to drive and regulation: satiety responsiveness, enjoyment of food and food responsiveness. Structural equation modeling was used to assess if those traits mediated the relationship between FTO and BMI z-score. The sample of children was 48.9% male and 91.0% non-Hispanic white. FTO distribution was in Hardy Weinberg equilibrium, and 16.3% of participants were homozygous for the high-risk allele. Mean BMI z-score was greatest among those with the high-risk genotype (ANOVA P < 0.01). In separate structural equation models adjusted for the child's sex and maternal education, decreased satiety responsiveness and increased food responsiveness each partially mediated the positive association between the high-risk genotype and increased BMI z-score (P-value for each indirect effect <0.05). Continued research is needed to better understand how other known genetic obesity risk factors may impact appetitive traits among children.
| S-EPMC5569318 | biostudies-literature
Project description:Emerging evidence suggests that attributing one's weight to genetics may contribute to the adoption of obesogenic behaviors. We investigated whether weight-related genetic attributions were associated with weight change during a weight gain prevention intervention.Participants (n = 185) were from a randomized clinical trial of a digital health weight gain prevention intervention for black women ages 25-44 years with body mass index 25.0-34.9?kg/m(2). Weight-related genetic attributions (weight status attribution and weight loss attributions) were measured at baseline and 12 months.Among intervention participants, high genetic attribution for weight loss was associated with greater weight loss at 12 months (-2.7 vs. 0.5?kg) and 18 months (-3.0 vs. 0.9?kg). Among usual-care participants, high genetic attribution for weight status was associated with greater 18-month weight gain (2.9 vs. 0.3?kg). The intervention reduced the likelihood of high genetic attribution for weight loss at 12 months (P = 0.05). Change in the likelihood of genetic attribution was not associated with weight change over 12 months.Impact of genetic attributions on weight differs for those enrolled and not enrolled in an intervention. However, weight gain prevention intervention may reduce genetic attribution for weight loss.Genet Med 18 5, 476-482.
| S-EPMC4761333 | biostudies-literature
Project description:Not every participant responds with a comparable body weight loss to lifestyle intervention, despite the same compliance. Genetic factors may explain parts of this difference. Variation in fat mass and obesity-associated gene (FTO) is the strongest common genetic determinant of body weight. The aim of the present study was to evaluate the impact of FTO genotype differences in the link between improvement of fitness and reduction of body weight during a lifestyle intervention.We genotyped 292 healthy subjects for FTO rs8050136. Participants underwent a 9-month lifestyle intervention. Before and after intervention, aerobic fitness was tested by bicycle (VO2max) and treadmill spiroergometry (individual anaerobic threshold (IAT), subgroup of N = 192).Participants lost body weight (p < 0.0001) independent of FTO genotype (p = 0.5). There was a significant correlation between improvement in VO2max and decrease in body weight (p < 0.0001). FTO genotype interacted with this relationship (p = 0.0042 for VO2max, p = 0.0049 for IAT). When stratifying the cohort according to their improvement in VO2max, FTO obesity-risk A-allele carriers in the higher quartiles of improvement in fitness lost significantly less body weight.Our data reveal that genetic variation in FTO impacts on body weight reduction during lifestyle intervention only in subjects with marked improvement in aerobic fitness.
| S-EPMC5644850 | biostudies-literature
Project description:Maternal vitamin D deficiency during pregnancy may influence offspring kidney health. We aimed to examine the associations of 25-hydroxyvitamin D (25(OH)D) blood levels during fetal life with kidney outcomes at school age.This study was embedded in a population-based prospective cohort study among 4212 mother-child pairs. We measured maternal second trimester (18-25 weeks) and fetal cord blood (at birth) 25(OH)D levels. At a median age of 6.0 years, we measured children's combined kidney volume, glomerular filtration rate (eGFR) from creatinine and cystatin C serum levels, and microalbuminuria from albumin and creatinine urine levels.Of all mothers, 21.9% had severely deficient levels (25(OH)D <25.0?nmol/l), 25.7% had deficient levels (25.0-49.9?nmol/l), 25% had sufficient levels (50.0-74.9?nmol/l) and 27.4% had optimal levels (?75.0?nmol/l). Maternal 25(OH)D levels were not consistently associated with childhood combined kidney volume. Higher maternal 25(OH)D levels were associated with lower childhood eGFR (difference -0.94?ml/min per 1.73?m(2) (95% confidence interval, -1.73; -0.15) per 1 standard deviation (s.d.) increase in 25(OH)D). Maternal 25(OH)D levels were not associated with microalbuminuria. Cord blood 25(OH)D levels were not associated with childhood kidney outcomes. The associations of maternal 25(OH)D levels with childhood eGFR were partly explained by childhood vitamin D status.Our findings suggest that maternal 25(OH)D levels during pregnancy may influence childhood kidney outcomes. These results should be considered hypothesis generating. Further studies are needed to replicate the observations, to examine the underlying mechanisms and to identify the long-term clinical consequences.
| S-EPMC5576536 | biostudies-literature
Project description:AimWe tested the hypothesis that the obesity-associated FTO SNP rs9939609 would be associated with clinically significant weight gain (≥ 5% of initial body weight) in the first year of university; a time identified as high risk for weight gain.MethodsWe collected anthropometric data from university students (n = 1,411, mean age: 22.4 ± 2.5 years, 49.1% male) at the beginning and end of the academic year. DNA was analysed for FTO rs9939609. Associations of FTO genotype with BMI at baseline were analysed using ANCOVA, and with risk of 5% weight gain over follow-up with logistic regression; both analyses adjusting for age and sex. The alpha level was reduced to 0.0125 to account for multiple testing.ResultsUsing an additive model, FTO status was not associated with higher BMI at baseline (22.2 vs. 21.9 kg/m2, p = 0.059). Dropout was high but unrelated to genotype. Among the 310 (21.9%) completing follow-up, those with AT genotypes had twice the odds of ≥ 5% weight gain compared with TTs (OR = 2.05, 95% CI = 1.05-4.01, p = 0.036), but this was no longer significant after Bonferroni correction. There was a trend for AA carriers for ≥ 5% weight gain compared with TT carriers (p = 0.089), but sample size was small.ConclusionThis study provides nominal evidence for the genetic susceptibility hypothesis, but findings need to be replicated.
| S-EPMC4959463 | biostudies-literature
Project description:BackgroundIncreased weight gain during infancy is a risk factor for obesity and related diseases in later life. The aim of the present study was to investigate the association between socioeconomic status (SES) and weight gain during infancy, and to identify the factors mediating the association between SES and infant weight gain.MethodsSubjects were 2513 parent-child dyads participating in a cluster randomized controlled intervention study. Family SES was indexed by maternal education level. Weight gain in different time windows (infant age 0-3, 0-6, and 6-12 months) was calculated by subtracting the weight for age z-score (WAZ) between the two time-points. Path analysis was performed to examine the mediating pathways linking SES and infant weight gain.ResultsOn average, infants of low-educated mothers had a lower birth weight and caught-up at approximately 6 months. In the period of 0-6 months, infants with low-educated mothers had an 0.42 (95% CI 0.27-0.57) higher gain in weight for age z-score compared to children with high-educated mothers. The association between maternal education level and increased infant weight gain in the period of 0-6 months can be explained by infant birth weight, gestational age at child birth, duration of breastfeeding, and age at introduction of complementary foods. After adjusting all the mediating factors, there was no association between maternal education level and infant weight gain.ConclusionInfants with lower SES had an increased weight gain during the first 6 months of infancy, and the effect can be explained by infant birth weight, gestational age at child birth, and infant feeding practices.
| S-EPMC6214496 | biostudies-literature
Project description:The fat mass and obesity-associated (FTO) gene was genotyped for the participants in the Dose-Response to Exercise in postmenopausal Women (DREW) trial and analyses were performed to determine whether an FTO variant was associated with adiposity and cardiorespiratory fitness (CRF) before and after 6 months of moderate intensity exercise in white women (n = 234). The A/A homozygotes for rs8050136 had a higher BMI (kg/m(2)) compared to C/C homozygotes at baseline (32.8 (0.6) vs. 31.0 (0.4), respectively; P < 0.05) and at follow-up (31.9 (0.6) vs. 30.4 (0.5), respectively; P < 0.05). Weight loss occurred after exercise, but there was no significant genotype by exercise interaction over time. Exploratory analyses among women exposed to moderate intensity exercise meeting, or exceeding, the physical activity recommendation found that those homozygous A/A lost significantly more weight than the C allele carriers (-3.3 (0.7) kg vs. -1.4 (0.4) kg and -1.5 (0.5) kg, respectively; P < 0.05). CRF, defined as VO(2peak) (oxygen consumption), increased after exercise and the magnitude of the increase was similar for each genotype. In conclusion, women genetically predisposed to being obese experienced weight loss and CRF benefits with moderate intensity exercise, with additional weight loss observed when the women met or exceeded the physical activity recommendations.
| S-EPMC2828508 | biostudies-literature
Project description:BackgroundExcessive pregnancy weight gain is associated with obesity in the offspring, but this relationship may be confounded by genetic and other shared influences. We aimed to examine the association of pregnancy weight gain with body mass index (BMI) in the offspring, using a within-family design to minimize confounding.Methods and findingsIn this population-based cohort study, we matched records of all live births in Arkansas with state-mandated data on childhood BMI collected in public schools (from August 18, 2003 to June 2, 2011). The cohort included 42,133 women who had more than one singleton pregnancy and their 91,045 offspring. We examined how differences in weight gain that occurred during two or more pregnancies for each woman predicted her children's BMI and odds ratio (OR) of being overweight or obese (BMI≥85th percentile) at a mean age of 11.9 years, using a within-family design. For every additional kg of pregnancy weight gain, childhood BMI increased by 0.0220 (95% CI 0.0134-0.0306, p<0.0001) and the OR of overweight/obesity increased by 1.007 (CI 1.003-1.012, p = 0.0008). Variations in pregnancy weight gain accounted for a 0.43 kg/m(2) difference in childhood BMI. After adjustment for birth weight, the association of pregnancy weight gain with childhood BMI was attenuated but remained statistically significant (0.0143 kg/m(2) per kg of pregnancy weight gain, CI 0.0057-0.0229, p = 0.0007).ConclusionsHigh pregnancy weight gain is associated with increased body weight of the offspring in childhood, and this effect is only partially mediated through higher birth weight. Translation of these findings to public health obesity prevention requires additional study. Please see later in the article for the Editors' Summary.
| S-EPMC3794857 | biostudies-literature