Dataset Information

MC3R gene polymorphisms are associated with early childhood adiposity gain and infant appetite in an Asian population.

ABSTRACT: BACKGROUND:Polymorphic variants within human melanocortin-3 receptor gene (MC3R) gene have been associated with obesity. However, its influence on infancy and early childhood adiposity has not been reported before. OBJECTIVES:We assessed associations between genotype at polymorphic sites within MC3R with early childhood adiposity and interaction with early childhood appetitive traits. METHODS:We studied 1090 singletons in an Asian mother-offspring cohort genotyped for MC3R and in a subgroup (n?=?422) who had completed Child Eating Behaviour Questionnaires (CEBQ) at 12 months. Children were followed from birth to 48 months, and up to 10 measurements of body mass index and five measures of triceps and subscapular skin-folds were obtained. RESULTS:Independent of potential confounders, each additional MC3R minor allele copy was associated with greater body mass index standard deviation score [B{95% confidence interval}: 0.004?units/month {0.001,0.007}; p?=?0.007], triceps [0.009?mm/month {0.001,0.02}; p?=?0.021] and subscapular skin-fold [0.008?mm/month {0.002,0.01}; p?=?0.011] gain velocity in the first 48 months. Each additional MC3R minor allele copy was also associated with increased odds of overweight [odds ratio {95% confidence interval}: 1.48{1.17-1.88}] and obesity [1.58{1.10-2.28}] in the first 48 months. Every additional copy of MC3R minor allele was positively associated with 'slowness-in-eating' appetitive trait [0.24{0.06,0.39}, p?=?0.006]; however, the relationship between 'slowness-in-eating' with adiposity gain was not statistically significant. CONCLUSIONS:Our findings support the role of MC3R genetic variants in adiposity gain during early childhood.

SUBMITTER: Aris IM

PROVIDER: S-EPMC5111755 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature

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MC3R gene polymorphisms are associated with early childhood adiposity gain and infant appetite in an Asian population.

Aris I M IM Tint M T MT Teh A L AL Holbrook J D JD Quah P L PL Chong M F-F MF Lin X X Soh S E SE Saw S-M SM Kwek K K Godfrey K M KM Gluckman P D PD Chong Y S YS Lek N N Yap F F Lee Y S YS

Pediatric obesity 20151211 6

<h4>Background</h4>Polymorphic variants within human melanocortin-3 receptor gene (MC3R) gene have been associated with obesity. However, its influence on infancy and early childhood adiposity has not been reported before.<h4>Objectives</h4>We assessed associations between genotype at polymorphic sites within MC3R with early childhood adiposity and interaction with early childhood appetitive traits.<h4>Methods</h4>We studied 1090 singletons in an Asian mother-offspring cohort genotyped for MC3R ...[more]

PMID: 26663875

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Project description:Genome-wide association studies have identified genetic risks for obesity. These genetic risks influence development of obesity partly by accelerating weight gain in childhood. Research is needed to identify mechanisms to inform intervention. Cross-sectional studies suggest appetite traits as a candidate mechanism. Longitudinal studies are needed to test whether appetite traits mediate genetic influences on children's weight gain.To test whether genetic risk for obesity predicts accelerated weight gain in middle childhood (ages 4-8 years) and whether genetic association with accelerated weight gain is mediated by appetite traits.Longitudinal study of a representative birth cohort at the Trondheim Early Secure Study, Trondheim, Norway, enrolled at age 4 years during 2007 to 2008, with follow-ups at ages 6 and 8 years. Participants were sampled from all children born in 2003 or 2004 who attended regular community health checkups for 4-year-olds (97.2% attendance; 82.0% consent rate, n = 2475). Nine hundred ninety-five children participated at age 4 years, 795 at age 6 years, and 699 at age 8 years. Analyses included 652 children with genotype, adiposity, and appetite data.Outcomes were body mass index and body-fat phenotypes measured from anthropometry (ages 4, 6, and 8 years) and bioelectrical impedance (ages 6 and 8 years). Genetic risk for obesity was measured using a genetic risk score composed of 32 single-nucleotide polymorphisms previously discovered in genome-wide association studies of adult body mass index. Appetite traits were measured at age 6 years with the Children's Eating Behavior Questionnaire.Of the 652 genotyped child participants, 323 (49.5%) were female, 58 (8.9%) were overweight, and 1 (0.2%) was obese. Children at higher genetic risk for obesity had higher baseline body mass index and fat mass compared with lower genetic risk peers, and they gained weight and fat mass more rapidly during follow-up. Each SD increase in genetic risk score was associated with a 0.22-point increase in BMI at age-4 baseline (for the intercept, unstandardized path coefficient B = 0.22 [95% CI, 0.06-0.38]; P = .008. Children with higher genetic risk scores also gained BMI points more rapidly from ages 4 to 6 years (B = 0.11 [95% CI, 0.03-0.20]; P = .01 ; ? = 0.12) and from 6 to 8 years (B = 0.09 [95% CI, 0.00-0.19]; P = .05; ? = 0.10), compared with their lower genetic risk peers. Children at higher genetic risk had higher levels of alleged obesogenic appetite traits than peers with lower genetic risk at age 6 years, but appetite traits did not mediate genetic associations with weight gain. The sum of the 5 indirect effects was B = -0.001 (95% CI, -0.02 -0.01); P = .86; ? = 0.00.Genetic risk for obesity is associated with accelerated childhood weight gain. Interventions targeting childhood weight gain may provide one path to mitigating genetic risk. However, middle childhood appetite traits may not be a promising target for such interventions. Studies of early-childhood samples are needed to test whether appetite traits explain how genetic risks accelerate growth earlier in development.

Project description:Background: Infant body mass index (BMI) peak has received much interest recently as a potential predictor of future obesity and metabolic risk. No studies, however, have examined infant BMI peak in Asian populations, in whom the risk of metabolic disease is higher.Methods: We utilized data among 1020 infants from a mother-offspring cohort, who were Singapore citizens or permanent residents of Chinese, Malay or Indian ethnicity with homogeneous parental ethnic backgrounds, and did not receive chemotherapy, psychotropic drugs or have diabetes mellitus. Ethnicity was self-reported at recruitment and later confirmed using genotype analysis. Subject-specific BMI curves were fitted to infant BMI data using natural cubic splines with random coefficients to account for repeated measures in each child. We estimated characteristics of the child's BMI peak [age and magnitude at peak, average pre-peak velocity (aPPV)]. Systolic (SBP) and diastolic blood pressure (DBP), BMI, sum of skinfolds (SSF) and fat-mass index (FMI) were measured during a follow-up visit at age 48 months. Weighted multivariable linear regression was used to assess the predictors (maternal BMI, gestational weight gain, ethnicity, infant sex, gestational age, birthweight-for-gestational age and breastfeeding duration) of infant BMI peak and its associations with outcomes at 48 months. Comparisons between ethnicities were tested using Bonferroni post-hoc correction.Results: Of 1020 infants, 80.5% were followed up at the 48-month visit. Mean (SD) BMI, SSF and FMI at 48 months were 15.6 (1.8) kg/m 2 , 16.5 (5.3) mm and 3.8 (1.3) kg/m 2 , respectively. Mean (SD) age at peak BMI was 6.0 (1.6) months, with a magnitude of 17.2 (1.4) kg/m 2 and pre-peak velocity of 0.7 (0.3) kg/m 2 /month. Compared with Chinese infants, the peak occurred later in Malay {B [95% confidence interval (CI): 0.64 mo (0.36, 0.92)]} and Indian infants [1.11 mo (0.76, 1.46)] and was lower in magnitude in Indian infants [-0.45 kg/m 2 (-0.69, -0.20)]. Adjusting for maternal education, BMI, gestational weight gain, ethnicity, infant sex, gestational age, birthweight-for-gestational-age and breastfeeding duration, higher peak and aPPV were associated with greater BMI, SSF and FMI at 48 months. Age at peak was positively associated with BMI at 48 months [0.15 units (0.09, 0.22)], whereas peak magnitude was associated with SBP [0.17 units (0.05, 0.30)] and DBP at 48 months [0.10 units (0.01, 0.22)]. Older age and higher magnitude at peak were associated with increased risk of overweight at 48 months [Relative Risk (95% CI): 1.35 (1.12-1.62) for age; 1.89 (1.60-2.24) for magnitude]. The associations of BMI peak with BMI and SSF at 48 months were stronger in Malay and Indian children than in Chinese children.Conclusions: Ethnic-specific differences in BMI peak characteristics, and associations of BMI peak with early childhood cardio-metabolic markers, suggest an important impact of early BMI development on later metabolic outcomes in Asian populations.

Project description:ObjectiveSmall birth size and rapid postnatal growth have been associated with higher future blood pressure. The timing of these effects, the relative importance of weight gain and linear growth and the role of infant feeding need to be clarified.MethodsWe assessed how blood pressure relates to birth weight, infant and childhood growth and infant feeding (duration of exclusive breastfeeding and timing of introduction of complementary feeding) in 2227 children aged 5 years from a prospective cohort study (Amsterdam Born Children and their Development). Postnatal growth was represented by statistically independent measures of relative weight gain (weight gain independent of height) and linear growth in four age periods during infancy (0-1 month; 1-3 months; 3-6 months; 6-12 months) and from 12 months to 5 years.ResultsLower birth weight was associated with higher childhood diastolic blood pressure (-0.38 mm Hg.SD-1; P = 0.007). Faster relative weight gain and linear growth after 1 month were positively associated with systolic and diastolic blood pressure. Associations of linear growth with systolic blood pressure ranged from 0.47 to 1.49 mm Hg.SD-1; P<0.01 for all. Coefficients were similar for different periods of infancy and also for relative weight gain and linear growth. Compared to breastfeeding <1 month, breastfeeding >1 month was associated with lower blood pressure (e.g. >6 months -1.56 mm Hg systolic blood pressure; P<0.001). Compared to >6 months, introduction of complementary feeding <6 months was associated with higher blood pressure (e.g. 4-6 months 0.91 mm Hg systolic blood pressure; P = 0.004).ConclusionsAfter the age of one month faster growth in either weight or height is associated with higher childhood blood pressure. It is unknown whether faster weight gain and linear growth carry the same risk for adult hypertension and cardiovascular morbidity. Longer breastfeeding and delayed introduction of complementary feeding may be associated with lower adult blood pressure.

Project description:BackgroundPotentially driven by the lack of mother-to-infant transmission of microbiota at birth, cesarean delivery has been associated with higher risk of offspring obesity. Yet, no studies have examined when delivery-mode differences in adiposity begin to emerge. In this study, we examine differences in infant weight and adiposity trajectories from birth to 12 months by delivery mode.MethodsFrom 2013 to 2015, we recruited pregnant women into the Nurture Study and followed up their 666 infants. We ascertained maternal delivery method and infant birth weight from medical records. We measured weight, length, and skinfold thicknesses (subscapular, triceps, abdominal) when infants were 3, 6, 9, and 12 months of age. The main outcome, infant weight-for-length z score, was derived based on the WHO Child Growth Standards. We used linear regression models to assess the difference at each time point and used linear mixed models to examine the growth rate for infant weight and adiposity trajectories. We controlled for maternal age, race, marital status, education level, household income, smoking status, maternal pre-pregnancy body mass index, and infant birth weight.ResultsOf the 563 infants in our final sample, 179 (31.8%) were cesarean delivered. From birth to 12 months, the rate of increase in weight-for-length z score was 0.02/month (p = 0.03) greater for cesarean-delivered than vaginally-delivered infants. As a result of more rapid growth, cesarean-delivered infants had higher weight-for-length z score (0.26, 95% CI: 0.05, 0.47) and sum of subscapular and triceps (SS + TR) skinfold thickness (0.95 mm, 95% CI: 0.30, 1.60)-an indicator for overall adiposity-at 12 months, compared to vaginally-delivered infants.ConclusionsCompared to vaginal delivery, cesarean delivery was associated with greater offspring rate of weight gain over the first year and differences in adiposity that appear as early as 3 months of age. Monitoring cesarean-delivered infants closely for excess weight gain may help guide primordial prevention of obesity later in life.

Dataset Information

MC3R gene polymorphisms are associated with early childhood adiposity gain and infant appetite in an Asian population.

Publications

MC3R gene polymorphisms are associated with early childhood adiposity gain and infant appetite in an Asian population.

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