The FTO rs9939609 polymorphism and obesity risk in teens: Evidence-based meta-analysis

Silva, Tainara Emilia Rodrigues da; Andrade, Nayara Lopes; Cunha, Daiane de Oliveira; Leão-Cordeiro, Jacqueline Andréia Bernardes; Vilanova-Costa, Cesar Augusto Sam Tiago; Silva, Antônio Márcio Teodoro Cordeiro

doi:10.1016/j.orcp.2018.08.001

Cited by 19 publications

(7 citation statements)

References 33 publications

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“…Polymorphisms in FTO and MC4R have been associated with obesity in children. A recent meta-analysis which included 13 articles published between 2011 and 2015, comprising 15,613 participants, shows that the polymorphism rs9939609 in FTO was significantly associated with an increased risk of obesity in children and adolescents in several populations, except Mexicans [23]. Another recent report exposed that the rs9939609 polymorphism interacts with the Native American-origin polymorphism rs9282541, in the ATP-binding cassette transporter ( ABCA1 ).…”

Section: Discussionmentioning

confidence: 99%

Polymorphisms in Adipokines in Mexican Children with Obesity

Jiménez-Osorio

Aguilar-Lucio

Cárdenas-Hernández

et al. 2019

International Journal of Endocrinology

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The high prevalence of childhood obesity in Mexico is alarming in the health-science field. We propose to investigate the contribution of adipokines and cytokines polymorphisms and common BMI/obesity-associated loci, revealed in genome-wide association studies in Caucasian adult cohorts, with childhood obesity. This study included 773 Mexican-Mestizo children (5-15 years old) in a case-control study. The polymorphisms included were ADIPOQ (rs6444174), TNF-α (rs1800750), IL-1β (rs1143643), IL-6 (rs1524107; rs2069845), NEGR1 (rs34305371), SEC16B-RASAL2 (rs10913469), TMEM18 (rs6548238; rs7561317), GNPDA2 (rs16857402), LEP (rs2167270), MTCH2 (rs10838738), LGR4-LIN7C-BDNF (rs925946), BCDIN3D-FAIM2 (rs7138803), FTO (rs62033400), MC4R (rs11872992), MC4R (rs17782313), and KCTD15 (rs29942). No significant contribution was found with adipokines and cytokines polymorphisms in this study. Only both TMEM18 (rs6548238; rs7561317) polymorphisms were found associated with obesity (OR=0.5, P=0.008) and were in linkage disequilibrium (r2=0.87). The linear regression showed that the rs7561317 polymorphism of TMEM18 is negatively associated with obesity. This report highlights the influence of TMEM18 in Mexican-Mestizo children obesity, while adipokine and cytokine polymorphisms were not associated with it.

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Section: Discussionmentioning

confidence: 99%

Polymorphisms in Adipokines in Mexican Children with Obesity

Jiménez-Osorio

Aguilar-Lucio

Cárdenas-Hernández

et al. 2019

International Journal of Endocrinology

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“…Although the impact of environmental factors, like a sedentary lifestyle and excessive nutrient supply, has a large contribution to the end result, more attention should be paid to other relevant obesity-related factors [ 4 ]. Many studies, also in the pediatric population, focus on single nucleotide polymorphisms (SNPs) in genes with a well-described relationship with obesity, such as FTO [ 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 ], or genes, whose role in obesity is recently gradually being discovered, as the PLAG1 gene [ 16 , 17 , 18 ]. However, very few studies address the impact of epigenetics, including the DNA methylation of CpG dinucleotides, on this phenomenon [ 19 , 20 ].…”

Section: Introductionmentioning

confidence: 99%

Methylation and Expression of FTO and PLAG1 Genes in Childhood Obesity: Insight into Anthropometric Parameters and Glucose–Lipid Metabolism

Czogała

Strojny

et al. 2021

Nutrients

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The occurrence of childhood obesity is influenced by both genetic and epigenetic factors. FTO (FTO alpha-ketoglutarate dependent dioxygenase) is a gene of well-established connection with adiposity, while a protooncogene PLAG1 (PLAG1 zinc finger) has been only recently linked to this condition. We performed a cross-sectional study on a cohort of 16 obese (aged 6.6–17.7) and 10 healthy (aged 11.4–16.9) children. The aim was to evaluate the relationship between methylation and expression of the aforementioned genes and the presence of obesity as well as alterations in anthropometric measurements (including waist circumference (WC), body fat (BF_kg) and body fat percent (BF_%)), metabolic parameters (lipid profile, blood glucose and insulin levels, presence of insulin resistance) and blood pressure. Expression and methylation were measured in peripheral blood mononuclear cells using a microarray technique and a method based on restriction enzymes, respectively. Multiple regression models were constructed to adjust for the possible influence of age and sex on the investigated associations. We showed significantly increased expression of the FTO gene in obese children and in patients with documented insulin resistance. Higher FTO expression was also associated with an increase in WC, BF_kg, and BF_% as well as higher fasting concentration of free fatty acids (FFA). FTO methylation correlated positively with WC and BF_kg. Increase in PLAG1 expression was associated with higher BF%. Our results indicate that the FTO gene is likely to play an important role in the development of childhood adiposity together with coexisting impairment of glucose-lipid metabolism.

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“…Additionally, the authors reported significantly higher levels of serum leptin ( p = 0.009) in A allele carriers (22.4 ± 0.9 ng mL −1 ) than those carrying the T/T genotype (17.4 ± 1.1 ng mL −1 ) [ 78 ]. Many other studies showed similar results, and a meta-analysis by da Silva et al showed that the TT genotype carried a significantly decreased risk of developing obesity in teens [ 79 ]. A better understanding of this key diet–gene interaction may be essential for the development of novel therapeutic approaches to address obesity.…”

Section: Genetic Testing and Nutrigeneticsmentioning

confidence: 74%

Genomics in Personalized Nutrition: Can You “Eat for Your Genes”?

et al. 2020

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Genome-wide single nucleotide polymorphism (SNP) data are now quickly and inexpensively acquired, raising the prospect of creating personalized dietary recommendations based on an individual’s genetic variability at multiple SNPs. However, relatively little is known about most specific gene–diet interactions, and many molecular and clinical phenotypes of interest (e.g., body mass index [BMI]) involve multiple genes. In this review, we discuss direct to consumer genetic testing (DTC-GT) and the current potential for precision nutrition based on an individual’s genetic data. We review important issues such as dietary exposure and genetic architecture addressing the concepts of penetrance, pleiotropy, epistasis, polygenicity, and epigenetics. More specifically, we discuss how they complicate using genotypic data to predict phenotypes as well as response to dietary interventions. Then, several examples (including caffeine sensitivity, alcohol dependence, non-alcoholic fatty liver disease, obesity/appetite, cardiovascular, Alzheimer’s disease, folate metabolism, long-chain fatty acid biosynthesis, and vitamin D metabolism) are provided illustrating how genotypic information could be used to inform nutritional recommendations. We conclude by examining ethical considerations and practical applications for using genetic information to inform dietary choices and the future role genetics may play in adopting changes beyond population-wide healthy eating guidelines.

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The FTO rs9939609 polymorphism and obesity risk in teens: Evidence-based meta-analysis

Cited by 19 publications

References 33 publications

Polymorphisms in Adipokines in Mexican Children with Obesity

Polymorphisms in Adipokines in Mexican Children with Obesity

Methylation and Expression of FTO and PLAG1 Genes in Childhood Obesity: Insight into Anthropometric Parameters and Glucose–Lipid Metabolism

Genomics in Personalized Nutrition: Can You “Eat for Your Genes”?

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