Open AccessProgramming of obesity and pediatric metabolic syndromes: a review in light of epigenetic modulation
Author(s) -
Liana Carla Albuquerque Peres Martinho
Publication year - 2021
Publication title -
international journal of nutrology
Language(s) - English
Resource type - Journals
eISSN - 2595-2854
pISSN - 1984-3011
DOI - 10.54448/ijn22104
Subject(s) - epigenetics , epigenome , obesity , dna methylation , metabolic syndrome , cpg site , bioinformatics , medicine , childhood obesity , biology , genetics , gene , gene expression , overweight
Obesity is a multifactorial health problem characterized by the excessive accumulation of fat in the body and affects approximately 338 million children and adolescents worldwide. For this reason, this study consisted of a literature review to investigate how the causes and treatments of pediatric obesity are being addressed in light of epigenetic modulation as a factor in metabolic programming. For this, preferentially original articles published in English between the years 2017 to 2021 in the PubMed and Scholar Google databases were searched using the epigenetics descriptors; epigenetic modulation; child obesity; metabolic syndrome, combined with each other. A total of 54,000 articles were returned to searches in PubMed and 16,107,000 in Scholar Google. Fewer than 500 studies jointly addressed epigenetics and aspects of obesity or metabolic syndromes in childhood. Only 14 works matched the search criteria. The most discussed epigenetic mechanism in the literature is DNA methylation, whose rates observed mainly in CpG islands of promoter regions in several genes contribute to the prevention and early diagnosis of obesity and other pediatric comorbidities even before birth, based on the correlation between the epigenetic marks, maternal and paternal health and anthropometric indices. Although experimental studies on infant metabolic programming are scarce, existing knowledge suggests that environmental, nutritional, and energy expenditure changes are capable of modulating the epigenome and reversing marks that induce susceptibility to metabolic comorbidities.