MC3R gene polymorphisms are associated with early childhood adiposity gain and infant appetite in an Asian population
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Updated: Mar 28, 2026

Sample Preparation to Bioinformatics Analysis of DNA Methylation: Association Strategy for Obesity and Related Trait Studies
Published on: May 6, 2022
I M Aris1,2, M T Tint3, A L Teh1
1Singapore Institute for Clinical Sciences, Agency for Science, Technology and Research, Singapore.
Insights
Genetic variants in the melanocortin-3 receptor gene (MC3R) are linked to increased childhood adiposity. This study shows MC3R influences early childhood body mass and obesity risk.
Area of Science:
- Genetics
- Pediatrics
- Metabolic Disorders
Background:
- Polymorphic variants in the human melanocortin-3 receptor gene (MC3R) have been linked to obesity.
- The impact of MC3R variants on infant and early childhood adiposity remains under-explored.
Purpose of the Study:
- To investigate the association between MC3R gene polymorphisms and early childhood adiposity.
- To examine potential interactions between MC3R genotype and appetitive traits in early childhood.
Main Methods:
- A cohort of 1090 Asian mother-offspring pairs were genotyped for MC3R.
- Childhood body mass index (BMI) and skinfold thickness were measured up to 48 months.
- Child Eating Behaviour Questionnaires (CEBQ) were administered to a subgroup at 12 months.
Main Results:
- Each additional MC3R minor allele copy correlated with increased BMI standard deviation score and skinfold thickness gain velocity.
- MC3R minor allele copy was associated with higher odds of overweight and obesity in early childhood.
- A positive association was found between MC3R minor allele and 'slowness-in-eating' trait, but not significantly with adiposity gain.
Conclusions:
- MC3R genetic variants play a role in adiposity accumulation during early childhood.
- Findings highlight the importance of MC3R in early life metabolic programming.
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.
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