Abstract

Introduction: Childhood obesity is occurring at alarming rates in both developed and developing countries. “Obesogenic” environmental factors must be associated with variants of different risk alleles to determine polygenic or common obesity, and their impact depends on different developmental stages.The interaction between obesogenic environment and genetic susceptibility results in the so-called polygenic forms of obesity. In contrast, monogenic and syndromic obesity are not influenced by environmental events. Therefore, this review aimed to underline the roles of some of the most studied genes in the development of monogenic and polygenic obesity in children.Results: Among the most common obesity related genes, we chose the fat mass and obesity-associated (FTO) gene, leptin gene and its receptor, tumor necrosis factor alpha (TNF-α), the melanocortin 4 receptor gene (MC4R), Ectoenzyme nucleotide pyrophosphate phosphodiesterase 1 (ENPP1), and others, such as peroxisome proliferator-activated receptor gamma (PPARG), angiotensin-converting enzyme (ACE), glutathione S-transferase (GST), and interleukin-6 (IL-6) genes. The roles of these genes are complex and interdependent, being linked to different cornerstones in obesity development, such as appetite behavior, control of food intake and energy balance, insulin signaling, lipid and glucose metabolism, metabolic disorders, adipocyte differentiation, and so on.Conclusions: Genetic predisposition is mandatory, but not enough to trigger obesity.Dietary interventions and proper lifestyle changes can prevent obesity development in genetically predisposed children. Further studies are needed to identify the precise role of both genetic and obesogenic factors in the development of childhood obesity in order to design effective preventive methods.

Highlights

  • Childhood obesity is occurring at alarming rates in both developed and developing countries

  • Silvenstoinen et al performed a systematic review on twins and adopted children and proved that environmental factors moderately influence body mass index (BMI) variation only up to the age of 13 years, their effect disappearing beyond this age [6]

  • The expression of genetic risks predominates during infancy and early childhood leading to an earlier adiposity rebound and higher BMI in children that carry a genetic susceptibility [17,18,19]

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Summary

Introduction

Childhood obesity is occurring at alarming rates in both developed and developing countries. In Romania, a recent study found that one in four children is overweight or obese and identified male sex, prepubertal age, and urban environment as risk factors for incidences of overweight [2] This major public health problem is a result of the interaction between environmental factors and individual genetic susceptibility. Silvenstoinen et al performed a systematic review on twins and adopted children and proved that environmental factors moderately influence BMI variation only up to the age of 13 years, their effect disappearing beyond this age [6] It is true BMI curve in children is genetically programmed, but at the same time environmental circumstances are able to modify this curve [8]. The expression of genetic risks predominates during infancy and early childhood leading to an earlier adiposity rebound and higher BMI in children that carry a genetic susceptibility [17,18,19]

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