RESUMO
Obesity develops largely due to genetic factors, with the genetic polymorphism of lipid metabolism enzymes being of particular importance. However, it is still unclear how the genetic variants of one of the key enzymes in lipid transport, lipoprotein lipase (LPL), are associated with the endocrine function of mesenchymal tissues in obesity. The current study was aimed at the investigation of the LPL rs328 gene variant association with adipokines and myokines levels, as well as lipid metabolism indices in the blood of children and adolescents of both genders with obesity. We found that LPL polymorphism rs328 is not characterized by the differences in the levels of hormones, adipokines, and myokines and in the blood of healthy children and adolescents; however, it significantly affects these indices during obesity in gender-dependent manner. The shifts in hormones, adipokines, and myokines manifest mostly in the obese individuals with Ser447Ser genotype rather than with 447Ter genotype. Obese boys homozygous for Ser447Ser have more elevated leptin levels than girls. They also demonstrate lower adiponectin, apelin, prolactin, and osteocrine levels than those in obese girls with the same genotype. The gender-based differences are less pronounced in individuals with 447Ter genotype than in the homozygotes for 447Ser. Thus, we conclude that the polymorphism rs328 of the lipoprotein lipase gene is accompanied by the changes in hormones, adipokines, and myokines levels in the blood of children and adolescents with obesity in gender-dependent manner.
Assuntos
Lipase Lipoproteica , Obesidade Infantil , Adolescente , Criança , Feminino , Humanos , Masculino , Adipocinas/sangue , Adiponectina , Genótipo , Lipase Lipoproteica/genética , Obesidade Infantil/genéticaRESUMO
Background: Obesity is one of the most common metabolic disorders in the world, which develops due to an imbalance in energy consumption and expenditure, and both genetic and environmental factors are of great importance. We investigated the potential interactions of single nucleotide polymorphisms that might contribute to the development of polygenic obesity in children. Objective: The study involved 367 children and adolescents of both sexes aged from 4 to 18 years. The control group (normal weight) and the overweight groups included 65 and 302 children respectively. Methods: DNA for analysis was isolated from peripheral blood lymphocytes, then allelic variants rs99305069 of the FTO gene (chr16:53786615), Gln192Arg of the PON1 gene (chr7: 95308134), -250G>A of the LIPC gene (chr15: 58431740), and Ser447Ter of the LPL gene (chr8:19957678) were studied using the SNP-Express reagent kit. The results of allelic interactions were analyzed using the multifactor dimensionality reduction method. Results and Discussion: Among overweight children, the distribution of genotype and allele frequencies for the studied single nucleotide polymorphisms of the four genes corresponded to those of the control group (p > 0.05). It was found that in obese children SerSer homozygotes at the Ser447Ter polymorphism of the LPL gene, had serum triglyceride (TG) levels 2.3 times higher than in children with the same genotype from the control group. In overweight Ser447Ter heterozygotes (p < 0.0001), the TG level exceeded the control values by only 13% (p = 0.044). A two-locus genotype FTO AT/LPL SerTer, was associated with a reduced risk of childhood obesity.