Author:
Fortes Jakeline S.,Pinto Renata M.,de Souza Raissa F.,Godoy Fernanda R.,da Cruz Raphael S.,de M e Silva Daniela,Filho Hugo P. Leite,da Cruz Aparecido D.,Minasi Lysa B.
Abstract
Abstract
Background
Obesity is defined as a multifactorial disease, marked by excessive accumulation of body fat, responsible for compromising the individual’s health over the years. The energy balance is essential for the proper functioning of the body, as the individual needs to earn and spend energy in a compensatory way. Mitochondrial Uncoupling Proteins (UCP) help in energy expenditure through heat release and genetic polymorphisms could be responsible for reducing energy consumption to release heat and consequently generate an excessive accumulation of fat in the body. Thus, this study aimed to investigate the potential association between six UCP3 polymorphisms, that have not yet been represented in ClinVar®, and pediatric obesity susceptibility.
Methods
A case–control study was conducted with 225 children from Central Brazil. The groups were subdivided into obese (123) and eutrophic (102) individuals. The polymorphisms rs15763, rs1685354, rs1800849, rs11235972, rs647126, and rs3781907 were determined by real-time Polymerase Chain Reaction (qPCR).
Results
Biochemical and anthropometric evaluation of obese group showed higher levels of triglycerides, insulin resistance, and LDL-C and low level of HDL-C. Insulin resistance, age, sex, HDL-C, fasting glucose, triglyceride levels, and parents’ BMI explained up to 50% of body mass deposition in the studied population. Additionally, obese mothers contribute 2 × more to the Z-BMI of their children than the fathers. The SNP rs647126 contributed to 20% to the risk of obesity in children and the SNP rs3781907 contribute to 10%. Mutant alleles of UCP3 increase the risk for triglycerides, total cholesterol, and HDL-C levels. The polymorphism rs3781907 is the only one that could not be a biomarker for obesity as the risk allele seem to be protective gains the increase in Z-BMI in our pediatric population. Haplotype analysis demonstrated two SNP blocks (rs15763, rs647126, and rs1685534) and (rs11235972 and rs1800849) that showed linkage disequilibrium, with LOD 76.3% and D’ = 0.96 and LOD 57.4% and D’ = 0.97, respectively.
Conclusions
The causality between UCP3 polymorphism and obesity were not detected. On the other hand, the studied polymorphism contributes to Z-BMI, HOMA-IR, triglycerides, total cholesterol, and HDL-C levels. Haplotypes are concordant with the obese phenotype and contribute minimally to the risk of obesity.
Publisher
Springer Science and Business Media LLC
Subject
Pediatrics, Perinatology and Child Health
Reference52 articles.
1. Sámano R, Huesca-Gómez C, López-Marure R, Hernández-Cabrera AK, Rodríguez-Ventura A, Tolentino M, et al. Association between UCP polymorphisms and adipokines with obesity in Mexican adolescents. J Pediatr Endocrinol Metab. 2018. https://doi.org/10.1515/jpem-2017-0262.
2. McPherson K. Reducing the global prevalence of overweight and obesity. Lancet. 2014. https://doi.org/10.1016/S0140-6736(14)60767-4.
3. Who.World Health Organization. Obesity: Preventing and managing the global epidemic. In: Report of a WHO Consultation on Obesity. Geneva: WHO; 1998. http://www.who.int/nutrition/publications/obesity/WHO_TRS_894/en/. Accessed 15 Jan 2021.
4. Wannmacher, L. Obesidade como fator de risco para morbidade e mortalidade: evidências sobre o manejo com medidas não medicamentosas. In: Uso Racional de Medicamentos: fundamentação em condutas terapêuticas e nos macroprocessos da Assistência Farmacêutica. Organização Pan-Americana da Saúde/Organização Mundial da Saúde (OPAS/OMS) no Brasil. 2016;1:7. https://www.paho.org/bra/dmdocuments/Fasciculo%207.pdf. Accessed 16 Jan 2021.
5. Grossman DC, Bibbins-Domingo K, Curry SJ, Barry MJ, Davidson KW, Doubeni CA, et al. Screening for obesity in children and adolescents: US preventive services task force recommendation statement. JAMA. 2017. https://doi.org/10.1001/jama.2017.6803.