In the present study, we identified the factors affected central obesity prevalence in the adult Altains, Russians and Tuvans permanently residing in the Altai and the Tuva Republics. The data was collected in 2018–2020. The examination program included anthropometrical examination and the genetic testing of females and males, aged 18–35 years. Anthropometrical examination was carried out in accordance with the guidelines accepted in the Research Institute and Museum of Anthropology. Body composition was analyzed by bioelectrical impedance analyzer. The SNPs rs1800592 UCP1, rs660339 UCP2 and rs1800849 UCP3 were assessed. The prevalence analyses of underweight, overweight and general obesity in the groups of female and males were conducted. The anthropometric indices were used to estimate the prevalence of central obesity. General obesity occurred more often in the group of Altai people, whereas in the Tuva people the central obesity is more pronounced. The Altai and Tuva people are alike in the total body measurements, whereas Russians were significantly higher. All studied groups demonstrated the sexual dimorphism of the body composition and waist to hip ratio. No significant differences in waist to height ratio between males and females were identified in the studied groups. No association between genetic variants and the obesity-related traits, which reflect the body fat and its distribution, was revealed. All factors included in the model are able to predict 8 % of the variability of the central obesity-related traits. Ethnic background contributes the most to the variability of the central obesity index.

Contribution of UCP1 single nucleotide polymorphisms (SNPs) to susceptibility for cardiometabolic pathologies (CMP) and their involvement in specific risk factors for these conditions varies across populations. We tested whether UCP1 SNPs A-3826G, A-1766G, Ala64Thr and A-112C are associated with common CMP and their risk factors across Armenia, Greece, Poland, Russia and United Kingdom. This case-control study included genotyping of these SNPs, from 2,283 Caucasians. Results were extended via systematic review and meta-analysis. In Armenia, GA genotype and A allele of Ala64Thr displayed ~2-fold higher risk for CMP compared to GG genotype and G allele, respectively (p<0.05). In Greece, A allele of Ala64Thr decreased risk of CMP by 39%. Healthy individuals with A-3826G GG genotype and carriers of mutant allele of A-112C and Ala64Thr had higher body mass index compared to those carrying other alleles. In healthy Polish, higher waist-to-hip ratio (WHR) was observed in heterozygotes A-3826G compared to AA homozygotes. Heterozygosity of A-112C and Ala64Thr SNPs was related to lower WHR in CMP individuals compared to wild type homozygotes (p0.05). Concluding, the studied SNPs could be associated with the most common CMP and their risk factors in some populations.

SAYP and Bap170, subunits of the SWI/SNF remodeling complex, have the ability to support enhancer-dependent transcription when artificially recruited to the promoter on a transgene. We found that the phenomenon critically depends on two subunits of the Mediator kinase module, Med12 and Med13 but does not require the two other subunits of the module (Cdk8 and CycC) or other subunits of the core part of the complex. A cooperation of the above proteins in active transcription was also observed at endogenous loci, but the contribution of the subunits to the activity of a particular gene differed in different loci. The factors SAYP/Bap170 and Med12/Med13 did not form sufficiently stable interactions in the extract, and their cooperation was apparently local at regulatory elements, the presence of SAYP and Bap170 in a locus being necessary for stable recruitment of Med12 and Med13 to the locus. In addition to the above factors, the Nelf-A protein was found to participate in the process. The cooperation of the factors, independent of enzymatic activities of the complexes they are part of, appears to be a novel mechanism that maintains promoter activity and may be used in many loci of the genome. Extended intrinsically disordered regions of the factors were assumed to sustain the mechanism.