سامانه کنگره های دانشگاه علوم پزشکی و خدمات بهداشتی و درمانی آذربایجان غربی

صفحه اصلی / بیستمین همایش سالیانه بیماری های شایع گوارش و کبد کودکان ایران و دومین همایش بین المللی چاقی کودکان

Genetic and Epigenetic Determinants of Childhood Obesity: A Review of Molecular Pathways and Clinical Implications

نویسندگان :

Kiana Ghafourian¹ Kiyanoush Jafari² Faezeh Ghalichi³

1- دانشگاه علوم پزشکی مراغه 2- دانشگاه علوم پزشکی مراغه 3- دانشگاه علوم پزشکی مراغه

کلمات کلیدی :

obesity،Genetic،childhood،Polygenic،Epigenetic

چکیده :

Background and Aim: Childhood obesity is a complex condition that arises from the interplay between genetic susceptibility, epigenetic alterations, and environmental factors. Childhood obesity involves polygenic predispositions as well as gene-gene and gene-environment interactions, with increasing evidence that epigenetic changes induced by the environment, particularly during prenatal life and early postnatal development, are also involved in the etiology and pathogenesis of obesity. These molecular modifications influence pathways that control craving, energy metabolism, and fat deposition and inflammation. The aim of the present study was to assess the Molecular Pathways and Clinical Implications of Genetic and Epigenetic Factors in Childhood Obesity. Methods: Related studies were retrieved from PubMed, Scopus and Web of Science published up to 2024. The following terms were used for searching related literature: obesity, childhood, epigenetic, genetic. We reviewed genetic polymorphisms, epigenetic mechanisms, and environmental obesogenic exposures. Results: According to research , fat mass and obesity-associated (FTO), Melanocortin 4 receptor, Leptin, and Brain-Derived Neurotrophic Factor gene polymorphisms were consistently positively associated with body mass index, appetite dysregulation, and energy imbalance and central adiposity. FTO alleles were associated with reduced satiety and increased caloric consumption. Epigenetic changes displayed anomalous DNA methylation in Leptin, Pro-opiomelanocortin, Adiponectin Q, and Hypoxia Inducible Factor 3 Subunit Alpha, which was associated with adiposity and metabolic dysfunction. In addition, it was identified that miR-122, miR-33 and lncRNAs affect lipid metabolism and insulin resistance. Methylation of intrauterine exposures (bisphenol A, phthalates) were related to metabolic genes and multi-generational higher obesity risk. Furthermore, maternal obesity and smoking affected the offspring's epigenetics, leading to remarkably faster weight gain. Conclusion: Reprogramming of epigenetic pathways can modulate gene expression in response to environmental exposures during critical windows of development. Genomic and epigenetic profiling may be used for early identification of children at greatest risk to allow for personalized prevention strategies aimed at long-term metabolic health.