A FTO variant and risk of acute coronary syndrome

Hubacek, Jaroslav A.; Staněk, Vladimír; Gebauerová, M; Pilipčincová, Alexandra; Dlouhá, Dana; Poledne, R.; Aschermann, Michal; Skalická, Hana; Matoušková, J.; Krüger, Andreas; Pěnička, Martin; Hrabakova, Hana; Veselka, Josef; Hájek, Petr; Lánská, Věra; Adámková, Věra; Piťha, Jan

doi:10.1016/j.cca.2010.03.037

Cited by 58 publications

(45 citation statements)

References 33 publications

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“…An increased risk of cardiovascular disease associated with different FTO variants has been demonstrated previously in people with type II diabetes mellitus, 6,7 in men with abnormal glucose metabolism, 10 and in people at normal risk of cardiovascular disease. 8,9 Our results are in line with previous findings of increased CHD risk associated with FTO variants in both men and women. The association with BMI was in agreement with the original genome-wide association study identifying the rs9939609 FTO variant.…”

Section: Discussionsupporting

confidence: 92%

“…This is consistent with results of several previous studies also demonstrating an association between FTO genotype and cardiovascular disease not entirely dependent on BMI. [6][7][8][9][10] This suggests that the association may be explained by other effects of the FTO gene in addition to the effect on weight and adiposity or by secondary factors linked to obesity (eg, lipid, metabolic, inflammatory, hypertension). The extent of the association between FTO and many metabolic variables (including glucose, insulin, LDL-C, high-density lipoprotein cholesterol, triglycerides) has been shown to be consistent with the effect on BMI.…”

Section: Discussionmentioning

confidence: 99%

“…Since the discovery of variants in the fat mass-and obesityassociated gene (FTO) that predispose to obesity and type II diabetes mellitus mainly through an increase in fat mass, [1][2][3][4][5] several studies have also shown association between FTO variants and cardiovascular disease. [6][7][8][9][10] The exact mechanism by which FTO influences adiposity is unknown, but a central regulatory effect on appetite and energy intake has been suggested, whereas energy expenditure and physical activity (PA) levels seem unaffected. [11][12][13][14][15][16] The minor allele A of the singlenucleotide polymorphism (SNP) rs9939609 (T>A) has been associated with an atherogenic lipid profile, 6 elevated plasma C-reactive protein levels, 17 and hypertension, 18 and a study in >17 000 Europeans showed that the FTO association with a range of metabolic measures (including low-density lipoprotein cholesterol [LDL-C] and high-density lipoprotein cholesterol, triglycerides, glucose, and insulin) was entirely because of its effect on body mass index (BMI).…”

mentioning

confidence: 99%

“…19 Several studies suggest that the FTO association with cardiovascular disease is not entirely mediated by BMI or other obesity-related factors. [6][7][8][9][10] However, it is unknown whether there are additional effects of FTO that could explain the association with cardiovascular disease.…”

mentioning

confidence: 99%

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FTO Genotype, Physical Activity, and Coronary Heart Disease Risk in Swedish Men and Women

Gustavsson

Mehlig

Leander

et al. 2014

Circ Cardiovasc Genet

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Background-Variants in the fat mass-and obesity-associated gene (FTO) predisposing to obesity and diabetes mellitus have also been associated with cardiovascular disease. Physical activity has been suggested to attenuate the FTO effect on obesity, but it is unknown whether this is also true for cardiovascular disease. Therefore, we explored whether physical activity modifies the FTO association with coronary heart disease (CHD). Methods and Results-FTO rs9939609 (T>A) polymorphism was genotyped in 2 Swedish population-based case-control studies with 1743 CHD cases and 4402 population controls (25-74 years of age; 41% women). Leisure time physical activity was assessed by questionnaires, and 3 levels were defined: low, medium, and high. Overall, carriers of the FTO A allele had an increased risk of CHD (odds ratio, 1.20; 95% confidence interval, 1.06-1.37) adjusted for age, sex, study, and body mass index. Although A-allele carriers with low physical activity had the highest CHD risk (odds ratio, 3.30; 95% confidence interval, 2.44-4.46) compared with those with TT genotype and high activity, the effects of FTO genotype and physical activity on CHD risk were approximately additive, indicating the absence of additive interaction. The stratum-specific relative risks of CHD from the A allele in subjects with low, medium, and high physical activity were odds ratio 1.11 (95% confidence interval, 0.77-1.60), 1.22 (1.04-1.44), and 1.38 (1.06-1.80), respectively, but the suggested multiplicative interaction was not significant. Conclusions-FTO rs9939609 A-allele carriers have an increased CHD risk, and the association is not counteracted by increased physical activity. (Circ Cardiovasc Genet. 2014;7:171-177.)

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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FTO Genotype, Physical Activity, and Coronary Heart Disease Risk in Swedish Men and Women

Gustavsson

Mehlig

Leander

et al. 2014

Circ Cardiovasc Genet

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“…FTO transcript expression has been detected in all of the tissues tested, and is the highest in the brain (McTaggart et al, 2011;Xing et al, 2013), which plays an important role in regulating feed intake and energy expenditure, commensurate with perceived whole-body energy requirements (Richards and Proszkowiec-Weglarz, 2007). In humans, several single nucleotide polymorphisms (SNPs) of FTO that are associated with the body mass index (BMI) have been found, which contribute to obesity and related diseases (Hubacek et al, 2010;Binh et al, 2013). Jia et al (2012) reported that in chickens, FTO is related to glucose metabolism, body weight (BW), and fat content.…”

Section: Introductionmentioning

confidence: 99%

Association between FTO polymorphism in exon 3 with carcass and meat quality traits in crossbred ducks

et al. 2015

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ABSTRACT. The fat mass and obesity-associated gene (FTO) is an excellent candidate gene that affects energy metabolism. Single nucleotide polymorphisms (SNPs) in FTO are associated with carcass and meat quality traits in pigs, cattle, and rabbits. The aim of this study was to investigate the association between novel SNPs in the FTO coding region and carcass and meat quality traits in 95 crossbred ducks, using DNA sequencing. We found two transitions G/A (SNP 387 and 473) within exon 3. SNP 387 was a synonymous mutation, whereas SNP 473 was a missense mutation. Association analysis suggested that SNP g.387G>A was significantly associated with all of the carcass traits measured, the intramuscular fat content (IMF), cooking yield (CY), pH values 45 min after slaughter (pH45m), drip losses from the breast muscle, and the leg muscle (P < 0.05). For SNP g.473G>A, the genotype AA exhibited greater leg muscle weight than the genotypes GG or AG (P < 0.05). The D value suggested that the two SNPs exhibited strong linkage disequilibrium. Three haplotypes (G 1 G 2 , G 1 A 2 , and A 1 A 2 ) were significantly associated with IMF, CY, the a* value, and all of the carcass traits measured (P < 0.05). The results suggest W. Gan et al. 6700©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (2): 6699-6714 (2015) that FTO is a candidate locus that affects carcass and meat quality traits in ducks.

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APOL1 polymorphisms are not influencing acute coronary syndrome risk in Czech males

Hubacek,

Adamkova,

Lanska

et al. 2024

Molec Gen & Gen Med

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BackgroundThe highest mortality and morbidity worldwide is associated with atherosclerotic cardiovascular disease (ASCVD), which has in background both environmental and genetic risk factors. Apolipoprotein L1 (APOL1) variability influences the risk of ASCVD in Africans, but little is known about the APOL1 and ASCVD in other ethnic groups.MethodsTo investigate the role of APOL1 and ASCVD, we have genotyped four (rs13056427, rs136147, rs10854688 and rs9610473) APOL1 polymorphisms in a group of 1541 male patients with acute coronary syndrome (ACS) and 1338 male controls.ResultsIndividual APOL1 polymorphisms were not associated with traditional CVD risk factors such as smoking, hypertension or diabetes prevalence, with BMI values or plasma lipid levels. Neither individual polymorphisms nor haplotypes were associated with an increased risk of ACS nor did they predict total or cardiovascular mortality over the 10.2 ± 3.9 years of follow‐up.ConclusionsWe conclude that APOL1 genetic variability has no major effect on risk of ACS in Caucasians.

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A FTO variant and risk of acute coronary syndrome

Cited by 58 publications

References 33 publications

FTO Genotype, Physical Activity, and Coronary Heart Disease Risk in Swedish Men and Women

FTO Genotype, Physical Activity, and Coronary Heart Disease Risk in Swedish Men and Women

Association between FTO polymorphism in exon 3 with carcass and meat quality traits in crossbred ducks

APOL1 polymorphisms are not influencing acute coronary syndrome risk in Czech males

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