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Genetic variants of the glucagon-like receptor-1 in obesity

100%
Nikulina A.
European Journal of Clinical and Experimental Medicine
|
2023
|
issue 4
682-691
EN
Introduction and aim. Dysfunction of the glucagon-like peptide 1 (GLP-1)/GLP-1 receptor (GLP-1R) axis promotes obesity and metabolic disorders. The aim was to study the associations of the single nucleotide variants (SNV) GLP1R gene with proinflammatory cytokines and metabolic disorders in children with various obesity phenotypes. Material and methods. 252 children with obesity aged 6-18 years were examined. The first group (n=152) was represented by children with metabolically unhealthy obesity (MUO). The second group (n=100) consolidated of children with metabolically healthy obesity (MHO). Whole genome sequencing (CeGat, Germany) was performed in 52 children. Results. An association with the development of obesity was noted for T alleles rs61754624 (t=3.33) and rs10305457 (t=2.06); with MUO – for C alleles rs1042044 (t=2.23), rs1126476 (t=2.63), rs2235868 (t=2.82); T alleles rs61754624 (t=3.33), rs10305457 (t=2.06) GLP1R, p<0.05. In the MHO group, a correlation was found with the levels of pro-inflammatory markers IL-1β, IL-6 in the presence of the GA genotype SNV rs3765468; with hyperglycemia - GA genotype SNV rs6923761, CC genotype SNV rs1042044, AA rs6918287; hyperinsulinemia - GA genotype SNV rs3765468, GG rs10305421; triglyceridemia - AA rs6918287 of GLP1R. Conclusion. SNV rs1042044, rs3765468, rs6923761, s6918287, and rs rs10305421 GLP1R are associated with the development of MUO in individuals with MHO.
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Role of genetic modification of the PNPLA3 gene in predicting metabolically unhealthy obesity and metabolic associated fatty liver disease in children

63%
Abaturov A., Nikulina A.
European Journal of Clinical and Experimental Medicine
|
2023
|
issue 1
5-13
EN
Introduction and aim. Single nucleotide variants (SNV) of the patatin‐like phospholipase domain‐containing protein 3 (PNP-LA3) gene play an important role in hepatic lipid remodeling and lipogenesis de novo, which is associated with the development of metabolically unhealthy obesity (MUO) and metabolic associated fatty liver disease (MAFLD). The aim of the study was to define the contribution of SNV PNPLA3 gene to the development of MUO, complicated by MAFLD in children. Material and methods. 200 obese children aged 6-18 years were examined. The main group (n=118) was represented by children with MUO. The control group (n=82) consolidated of children with metabolically healthy obesity (MHO). Whole genome sequencing (CeGat) was performed in 31 children of the main and 21 children of the control group. Results. Among obese children, 14 variants of SNV PNPLA3 (rs139051, rs34179073, rs2294918, rs139047, rs779127153, rs2076212, rs738409, rs738408, rs4823173, rs2072906, rs2076213, rs141106484, rs138736228) were identified, including SNV PNPLA3 g.44322818, not described in the dbSNP core database. The role of the following SNV PNPLA3 genotypes in the development of MUO complicated by MAFLD was revealed: rs738409 C/G (Relative risk (RR)=1.71); rs738408 C/T (RR=1.71); rs4823173 G/A (RR=1.57); rs2072906 A/G (RR=1.57) with Sensitivity (Se)=0.63 and Specificity (Sp)=0.72. Conclusion. The contribution to the development of MUO complicated by MAFLD in children is made by the linked association of genotypes: rs738409 C/G, rs738408 C/T, rs4823173 G/A and rs2072906 A/G out of 14 PNPLA3 SNVs diagnosed by us.
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