DOI: https://doi.org/10.22141/2224-0551.15.4.2020.208476
Phenotypes of obesity in children, clinical manifestations and genetic associations
Abstract
The literature review presents modern ideas about molecular genetic features, clinical manifestations of phenotypes of obesity in children. The development of obesity results from the imbalance between energy intake and expenditure over a long period. Currently, among phenogenic obesity cases, two phenotypes are distinguished: one of which is characterized by the absence of metabolic disorders, called metabolically healthy obese (MHO), and the second, due to the presence of metabolic complications of obesity, is metabolically unhealthy obesity (metabolically unhealthy obese — MUO). The main genomic representatives that participate in the regulation of energy consumption are the genes ghrelin, leptin, leptin receptors, the gene associated with mass and obesity, the melanocortin 4 receptor gene, the glucagon-like peptide 1, and cholecystokinin. In contrast to the MHO phenotype, which is mainly due to changes in the activity of genes expressed in the brain; the MUO phenotype is associated with genes, most of which are mainly expressed in peripheral tissues. Genetic features of the expression of peripheral tissues involved in adipogenesis determine the distribution of excess adipose tissue: a predominant increase in the mass of subcutaneous adipose tissue leads to the development of the MHO phenotype, and excess weight of visceral and ectopic adipose tissue leads to the appearance of the MUO phenotype. Excess weight of subcutaneous fat does not lead to systemic metabolic disorders, but it is a transitional phenomenon in MHO, while visceral obesity and the accumulation of ectopic fat in the liver, pancreas, heart tissues and skeletal muscles are causally associated with low-grade inflammation, insulin resistance, impaired glucose metabolism and the development of cardiovascular disease and is typical for the MUO phenotype. The absence of generally accepted criteria for verifying the phenotype of obesity requires the search for new markers for identifying disorders of various metabolic pathways that would allow us to reliably distinguish MHO and MUO.
Keywords
obesity; phenotypes; genetic associations; children; review
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