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.
Keywords: children; dietary interventions; etiology; genetics; obesity.