Obesity‐related genetic polymorphisms and adiposity indices in a young Italian population

Jan 17, 2017IUBMB life

Genetic differences linked to obesity and body fat in young Italians

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Abstract

Minor allele homozygotes of MC4R rs17782313 and PPARG rs1801282 show significantly higher body mass index (BMI) and waist-to-height ratio (WHtR).

MC4R rs17782313 is associated with an increase in BMI by 1.258 and WHtR by 0.021.
PPARG rs1801282 is linked to an increase in BMI by 6.689 and WHtR by 0.069.
An epistatic interaction was identified between ACE and MC4R, suggesting heterozygosity at ACE rs4646994 may protect against weight gain associated with the MC4R C/C genotype.
The study highlights the complexity of genetic influences on obesity, particularly in young and athletic populations.
Further research is necessary to understand gene-gene interactions in obesity.

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Pediatric obesity develops when a complex biological predisposition collides with an obesogenic environment. To further elucidate the role of genetics in obesity onset, we performed a candidate-gene association study in a young and sportive Italian population by testing the association of functional polymorphisms in ACE (rs4646994), FTO (rs9939609), MC4R (rs17782313) and PPARG (rs1801282) genes with body mass index (BMI) and waist-to-height ratio (WHtR). We also tested the combinations of identified risk genotypes and epistatic interactions among them to determine the existence of cumulative effects in predicting the predisposition to gain weight. Our results confirm a significant direct influence of MC4R rs17782313 and PPARG rs1801282 on body composition, that is, minor allele homozygotes showed significantly higher BMI (rs17782313, β = 1.258, P = 0.031; rs1801282, β = 6.689, P = 1.2 × 10) and WHtR (rs17782313, β = 0.021, P = 0.005; rs1801282, β = 0.069, P = 0.003) values. Moreover, by leveraging multifactor dimensionality reduction and general linear model (GLM) approaches we identified an epistatic interaction between ACE and MC4R, where heterozygosity at ACE rs4646994 seems to protect from the unfavorable predisposition to gain weight given by C/C genotype at MC4R rs17782313 (GLM, P = 0.004). In conclusion, to clarify the role of genetics in multifactorial diseases remains a difficult goal, even for the most investigated polymorphisms and in controlled populations. Further studies on epistasis and gene-gene interaction will help to elucidate this complex scenario. © 2017 IUBMB Life, 69(2):98-105, 2017. -4

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Obesity‐related genetic polymorphisms and adiposity indices in a young Italian population

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