The Genetic Basis of Childhood Obesity: A Systematic Review

Overweight and obesity in childhood and adolescence represents one of the most challenging public health problems of our century owing to its epidemic proportions and the associated significant morbidity, mortality, and increase in public health costs. The pathogenesis of polygenic obesity is multif...

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Main Authors: Aikaterini Vourdoumpa, George Paltoglou, Evangelia Charmandari
Format: Article
Language:English
Published: MDPI AG 2023-03-01
Series:Nutrients
Subjects:
Online Access:https://www.mdpi.com/2072-6643/15/6/1416
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author Aikaterini Vourdoumpa
George Paltoglou
Evangelia Charmandari
author_facet Aikaterini Vourdoumpa
George Paltoglou
Evangelia Charmandari
author_sort Aikaterini Vourdoumpa
collection DOAJ
description Overweight and obesity in childhood and adolescence represents one of the most challenging public health problems of our century owing to its epidemic proportions and the associated significant morbidity, mortality, and increase in public health costs. The pathogenesis of polygenic obesity is multifactorial and is due to the interaction among genetic, epigenetic, and environmental factors. More than 1100 independent genetic loci associated with obesity traits have been currently identified, and there is great interest in the decoding of their biological functions and the gene–environment interaction. The present study aimed to systematically review the scientific evidence and to explore the relation of single-nucleotide polymorphisms (SNPs) and copy number variants (CNVs) with changes in body mass index (BMI) and other measures of body composition in children and adolescents with obesity, as well as their response to lifestyle interventions. Twenty-seven studies were included in the qualitative synthesis, which consisted of 7928 overweight/obese children and adolescents at different stages of pubertal development who underwent multidisciplinary management. The effect of polymorphisms in 92 different genes was assessed and revealed SNPs in 24 genetic loci significantly associated with BMI and/or body composition change, which contribute to the complex metabolic imbalance of obesity, including the regulation of appetite and energy balance, the homeostasis of glucose, lipid, and adipose tissue, as well as their interactions. The decoding of the genetic and molecular/cellular pathophysiology of obesity and the gene–environment interactions, alongside with the individual genotype, will enable us to design targeted and personalized preventive and management interventions for obesity early in life.
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spelling doaj.art-48b854766c04489fa2c31a1445675ed92023-11-17T13:05:30ZengMDPI AGNutrients2072-66432023-03-01156141610.3390/nu15061416The Genetic Basis of Childhood Obesity: A Systematic ReviewAikaterini Vourdoumpa0George Paltoglou1Evangelia Charmandari2Division of Endocrinology, Metabolism and Diabetes, First Department of Pediatrics, National and Kapodistrian University of Athens Medical School, ‘Aghia Sophia’ Children’s Hospital, 11527 Athens, GreeceDivision of Endocrinology, Metabolism and Diabetes, First Department of Pediatrics, National and Kapodistrian University of Athens Medical School, ‘Aghia Sophia’ Children’s Hospital, 11527 Athens, GreeceDivision of Endocrinology, Metabolism and Diabetes, First Department of Pediatrics, National and Kapodistrian University of Athens Medical School, ‘Aghia Sophia’ Children’s Hospital, 11527 Athens, GreeceOverweight and obesity in childhood and adolescence represents one of the most challenging public health problems of our century owing to its epidemic proportions and the associated significant morbidity, mortality, and increase in public health costs. The pathogenesis of polygenic obesity is multifactorial and is due to the interaction among genetic, epigenetic, and environmental factors. More than 1100 independent genetic loci associated with obesity traits have been currently identified, and there is great interest in the decoding of their biological functions and the gene–environment interaction. The present study aimed to systematically review the scientific evidence and to explore the relation of single-nucleotide polymorphisms (SNPs) and copy number variants (CNVs) with changes in body mass index (BMI) and other measures of body composition in children and adolescents with obesity, as well as their response to lifestyle interventions. Twenty-seven studies were included in the qualitative synthesis, which consisted of 7928 overweight/obese children and adolescents at different stages of pubertal development who underwent multidisciplinary management. The effect of polymorphisms in 92 different genes was assessed and revealed SNPs in 24 genetic loci significantly associated with BMI and/or body composition change, which contribute to the complex metabolic imbalance of obesity, including the regulation of appetite and energy balance, the homeostasis of glucose, lipid, and adipose tissue, as well as their interactions. The decoding of the genetic and molecular/cellular pathophysiology of obesity and the gene–environment interactions, alongside with the individual genotype, will enable us to design targeted and personalized preventive and management interventions for obesity early in life.https://www.mdpi.com/2072-6643/15/6/1416SNPsCNVsobesityBMIbody compositionlifestyle intervention
spellingShingle Aikaterini Vourdoumpa
George Paltoglou
Evangelia Charmandari
The Genetic Basis of Childhood Obesity: A Systematic Review
Nutrients
SNPs
CNVs
obesity
BMI
body composition
lifestyle intervention
title The Genetic Basis of Childhood Obesity: A Systematic Review
title_full The Genetic Basis of Childhood Obesity: A Systematic Review
title_fullStr The Genetic Basis of Childhood Obesity: A Systematic Review
title_full_unstemmed The Genetic Basis of Childhood Obesity: A Systematic Review
title_short The Genetic Basis of Childhood Obesity: A Systematic Review
title_sort genetic basis of childhood obesity a systematic review
topic SNPs
CNVs
obesity
BMI
body composition
lifestyle intervention
url https://www.mdpi.com/2072-6643/15/6/1416
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