Associations of the FTO rs9939609 and the MC4R rs17782313 polymorphisms with type 2 diabetes are modulated by diet, being higher when adherence to the Mediterranean diet pattern is low

Ortega-Azorín, Carolina; Sorlí, José V.; Asensio, Eva M.; Coltell, Óscar; Martínez‐González, Miguel Ángel; Salas‐Salvadó, Jordi; Covas, Marı́a-Isabel; Arós, Fernando; Lapetra, José; Serra-Majem, Lluís; Gómez‐Gracia, Enrique; Fiol, Miquel; Sáez, Guillermo T.; Pintó, Xavier; Muñoz, Miguel Ángel; Ros, Emilio; Ordovás, José M.; Estruch, Ramón; Corella, Dolores

doi:10.1186/1475-2840-11-137

Cited by 134 publications

(106 citation statements)

References 60 publications

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“…For example, Moore and co-workers 48 showed that the significant association between ENPP1 and increased incidence of T2DM was mediated by lifestyle or metformin intervention. Ortega-Azorin and co-workers 49 also found an interaction between FTO and mediterranean diet in determining T2DM, with carriers of the FTO-rs9939609 minor allele on a low Meddiet having a higher risk of prevalent T2DM than individuals homozygous for the major allele. In a European-American population group, Mattei and co-workers 50 observed a significant interaction between the TCF7L2-rs12255372-TT risk genotype and fat intake for changes in BMI, total fat mass, and trunk fat mass at 6 month of lifestyle intervention.…”

Section: Limitationsmentioning

confidence: 89%

Contribution of ENPP1, TCF7L2, and FTO polymorphisms to type 2 diabetes in mixed ancestry ethnic population of South Africa

et al. 2016

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Background: Transcription factor 7-like 2 gene (TCF7L2), fat mass and obesity-associated gene (FTO), and ectonucleotide pyrophosphatase/phosphodiesterase gene (ENPP1) are known risk loci for type 2 diabetes (T2DM) mostly in European populations. Objectives: To assess the association of these genes with T2DM risk in a South African mixed-ancestry population. Methods: Five hundred and sixty six participants were genotyped for ENPP1-rs997509 and -rs1044498, FTO-9941349 and -rs3751812, TCF7L2-rs12255372 and -rs7903146 polymorphisms using Taqman genotyping assays and validated by automated sequencing to assess the association of the polymorphisms with cardiometabolic traits. Results: In logistic regression models adjusted for age, sex, body mass index (BMI) and insulin resistance, minor allele of rs997509 was associated with a higher risk of prevalent T2DM under a recessive model [odd ratio 4.60 (95% confidence interval: 1.07 to 19.86); p = 0.040].Under additive model, the rs7903146 [1.43 (1.00 to 2.04); p= 0.053] and rs9941349 [1.43 (1.00 to 2.04); p = 0.052] minor alleles showed marginally significant associations with a high risk of T2DM. However, only the rs7903146 alleles (p=0.011) and genotypes (p=0.025) distributions were statistically significantly different between diabetic and non-diabetic individuals. Conclusion: Our findings demonstrate that ENPP1, TCF7L2, and FTO may predispose to T2DM in the mixed-ancestry population.

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Section: Limitationsmentioning

confidence: 89%

Contribution of ENPP1, TCF7L2, and FTO polymorphisms to type 2 diabetes in mixed ancestry ethnic population of South Africa

et al. 2016

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“…Ortega-Azorín et al (2012) found a significant gene-diet interaction of the FTO rs9939609 and MC4R rs17782313 polymorphisms with type 2 diabetes depending on diet, in which the Mediterranean diet counteracts the genetic predisposition. A cross-sectional study found that individuals carrying both AA risk allele of the rs9939609 polymorphism were positively associated with a high intake of total fat (>34% energy) and low fiber consumption (<16 g/day), independently of BMI (Steemburgo et al 2013).…”

Section: Preventionmentioning

confidence: 92%

Current review of genetics of human obesity: from molecular mechanisms to an evolutionary perspective

et al. 2015

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Although the prevalence of obesity is increasing in most countries, partially due to ubiquitous exposure to energy dense foods, not everyone exposed to the current obesogenic environment shows unhealthy weight gain. This suggests that there are marked differences in genetic factors that increase vulnerability for excess weight gain. Indeed, evidence suggests that 40 to 70% of variance in unhealthy weight gain can be attributed to individual genetic variations. Moreover, emerging data imply that genetic vulnerability factors interact with environment risk, which is referred to as an epigenetic process.Whereas most scholars consider obesity to be a disorder that results from the interaction between lifestyle and genetic factors, its origin is complex, poorly understood, and extent treatments are typically ineffective. Like any other aspect of science, our knowledge about the genetic basis of obesity is under constant revision. The current paper provides a review on the origins, mechanisms, evolutionary explanation, prevention and treatment based on genotyping.

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“…The Fat Mass and Obesity (FTO) gene is considered as leading obesity and type 2 diabetes [8]. The FTO rs9939609 minor allele, the risk allele for obesity, increased the risk of type 2 diabetes, this association remaining statistically significant even after adjustment for BMI [9].…”

Section: Discussionmentioning

confidence: 99%

The age of developing diabetes and FTO polymorphisms (rs9939609, rs1421085, and rs9930506)

Grzeszczak

Molsa

Tłuczykont

et al. 2017

Endokrynologia Polska

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Introduction: Type 2 diabetes (T2DM) is a common complex metabolic disorder that has a strong genetic predisposition. Fat mass and obesity-associated protein (FTO) is one of the genes of interest to us. Hypomethylation of a CpG site in the FTO gene was significantly associated with the risk of T2DM. The aim of the study was to find the answer to the question of whether the polymorphism changes of the FTO gene in the pathogenesis of type 2 diabetes are comparable in young, middle aged, and elderly people. Material and methods: The study involved 282 consecutive patients with type 2 diabetes, who attended a primary healthcare clinic in Southern Poland. The study subjects were divided into three groups according to the age at which type 2 diabetes mellitus was diagnosed (> 40 years old, 40-60 years old, and > 60 years old). The genotyping of rs9939609, rs1421085, and rs9930506 FTO polymorphisms was conducted using TaqManPre-designed SNP Genotyping Assay. Results: No statistically significant difference was shown between the examined FTO polymorphism (rs9939609, rs1421085, and rs9930506) distribution between the subjects diagnosed with diabetes < 40 years , 40-60 years, and > 60 years old. Conclusions: There were no statistically significant relationships between the different analysed anthropometric and other parameters and distribution of examined FTO polymorphisms (rs9939609 , rs1421085, and rs9930506). The age of diabetes was not affect by the tested FTO polymorphisms (rs9939609 , rs1421085, and rs9930506).

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Associations of the FTO rs9939609 and the MC4R rs17782313 polymorphisms with type 2 diabetes are modulated by diet, being higher when adherence to the Mediterranean diet pattern is low

Cited by 134 publications

References 60 publications

Contribution of ENPP1, TCF7L2, and FTO polymorphisms to type 2 diabetes in mixed ancestry ethnic population of South Africa

Contribution of ENPP1, TCF7L2, and FTO polymorphisms to type 2 diabetes in mixed ancestry ethnic population of South Africa

Current review of genetics of human obesity: from molecular mechanisms to an evolutionary perspective

The age of developing diabetes and FTO polymorphisms (rs9939609, rs1421085, and rs9930506)

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