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- Bennet, Louise, et al.
(författare)
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Dubbelt så hög risk för diabetes typ 2 hos svenskar födda i Irak
- 2015
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Ingår i: Läkartidningen. - 0023-7205. ; 112:16, s. 1-4
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- The MEDIM study reports that Immigrants from the Middle East to Sweden – independently of other diabetes related risk factors – have a twice as high type 2 diabetes risk as compared to non-immigrated Swedes. Diabetes onset occurs 6 years earlier in this group and is partly explained by family history and/or obesity. But the MEDIM study has identified that Middle Eastern background per se is an independent risk factor for earlier disease onset. Immigrants from the Middle East free of diabetes have a more pronounced insulin resistance and worse glycaemic control than non-immigrated Swedes independently of age, obesity or other risk factors for diabetes. To be able to reduce the risk of diabetes and offer an equal health care, glucose/HbA1c should be controlled on wide indications, and risk evaluation and preventive actions provided earlier for this population at high risk for type 2 diabetes. © 2015, Swedish Medical Association. All rights reserved.
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| 2. |
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| 3. |
- Chikowore, Tinashe, et al.
(författare)
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GWAS transethnic meta-analysis of BMI in similar to 700k individuals reveals novel gene-smoking interaction in African populations
- 2020
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Ingår i: Genetic Epidemiology. - : John Wiley & Sons. - 0741-0395 .- 1098-2272. ; 44:5, s. 475-476
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Sixty two percent of the 1.12 billion obese people globally reside in low‐middle income countries, 77% of which are in Africa. There is paucity of data on gene‐lifestyle interactions associated with the increasing prevalence of obesity among Africans. We hypothesised that gene‐environment interacting (GEI) variants exhibit heterogenous effects on obesity in transethnic meta‐analysis of marginal SNP associations as a result of modification by an unknown exposure that varies across populations.Body mass index (BMI) genome‐wide association study (GWAS) summary statistics for 678,671 individuals representative of the major global ancestries were aggregated at 21,338,816 SNPs via fixed‐effects meta‐analysis. Lead SNPs attaining genome‐wide significance (P < 5 × 10−8) were tested for heterogeneity in effects between GWAS. Lead SNPs with significant evidence of heterogeneity after Bonferroni correction were then selected for interaction analysis with selected lifestyle factors in an independent AWI‐Gen study of 10,500 African participants. Significant interaction findings were then replicated in 3,177 individuals of African ancestry in the UK Biobank.Of 881 lead SNPs, five had significant heterogenous effects on BMI (P < 5.7 × 10−5). Rs471094, at the CDKAL1 locus had significant interaction with smoking status, which reduced the effect of the BMI raising allele in current smokers (Betaint = −0.949 kg/m2; P int = .002) compared with non‐smokers in AWI‐Gen. This finding was validated in the UK Biobank (Betaint = −1.471 kg/m2, P int = .020; meta‐analysis Betaint = −1.050 kg/m2, P int = .0002). Our results highlight the first gene‐lifestyle interaction on BMI in Africans and demonstrate the utility of transethnic meta‐analysis of GWAS for identifying GEI effects.
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| 5. |
- Franks, Paul, et al.
(författare)
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Epigenetics and obesity: the devil is in the details
- 2010
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Ingår i: BMC Medicine. - : Springer Science and Business Media LLC. - 1741-7015. ; 8
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Obesity is a complex disease with multiple well-defined risk factors. Nevertheless, susceptibility to obesity and its sequelae within obesogenic environments varies greatly from one person to the next, suggesting a role for gene x environment interactions in the etiology of the disorder. Epigenetic regulation of the human genome provides a putative mechanism by which specific environmental exposures convey risk for obesity and other human diseases and is one possible mechanism that underlies the gene x environment/treatment interactions observed in epidemiological studies and clinical trials. A study published in BMC Medicine this month by Wang et al. reports on an examination of DNA methylation in peripheral blood leukocytes of lean and obese adolescents, comparing methylation patterns between the two groups. The authors identified two genes that were differentially methylated, both of which have roles in immune function. Here we overview the findings from this study in the context of those emerging from other recent genetic and epigenetic studies, discuss the strengths and weaknesses of the study and speculate on the future of epigenetics in chronic disease research. See research article: http://www.biomedcentral.com/1741-7015/8/87/abstract
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| 7. |
- Franks, Paul W.
(författare)
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Body Weight and Risk of Early Death
- 2013
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Ingår i: Obesity. - : Wiley-Blackwell. - 1930-7381 .- 1930-739X. ; 21:9, s. 1743-1743
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 8. |
- Franks, Paul W., et al.
(författare)
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Gene-diet interaction analysis, fine mapping and genomic annotation of the FADS1-2-3 gene cluster reveals regulatory potential in diabetes
- 2017
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Ingår i: Diabetologia. - : Springer. - 0012-186X .- 1432-0428. ; 60:1, s. S163-S163
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Background and aims: Polymorphisms at the fatty acid desaturase gene cluster (FADS1-FADS2-FADS3) have been associated with multiple metabolic and anthropometric traits in Greenlandic Inuit. We systematically assessed whether loci in the FADS region modify the association between dietary fat intake and cardiometabolic traits and functionally annotated top variants to estimate causal loci.Materials and methods: Data analyses consisted of: 1) interaction analyses between the six candidate genetic variants; 2) gene-centric joint analyses to detect interaction signals in the FADS region; 3) haplotype-centric joint tests across 30 haplotype blocks in the FADS1- 3 region to refine interaction signals: 4) functional annotation of top loci. These analyses were undertaken in Swedish adults from the GLACIER Study (N=5,160); data on gene variation (Metabochip array) and height, body weight, fasting and 2hr-glucose, triglycerides, and HDL-, LDL- and total cholesterol were available. Dietary intakes of n3, n-6 and total polyunsaturated fatty acids (PUFA) were calculated from food-frequency questionnaires. Results were adjusted for multiple testing.Results: SNP-level multiplicative interactions were observed between rs174570 and n-6 PUFA intake on fasting glucose (Pinteraction=0.007) and between rs174602 and n-3 PUFA intake on total cholesterol (Pinteraction=0.015). Gene-centric analyses demonstrated evidence for joint main and interaction effects for FADS on body weight (Pn-3.joint = 0.018, Pn-6.joint = 0.021, PPUFA.joint = 0.024) and on BMI (Pn-3.joint = 0.031, Pn-6.joint = 0.029, PPUFA.joint = 0.033) irrespective of types of fatty acid intake. An interaction was detected for FADS1-3 and n-3 PUFA on triglycerides (Pint=0.005). The haplotype analyses revealed three blocks (Pint ≤0.011) that drive the interaction between FADS1-3 and n-3 PUFA on triglycerides. Genomic annotation showed that the rs5792235 variant demonstrated the highest functionality score (Figure).Conclusion: The association between FADS1-3 variants and triglycerides may be modified by PUFA intake. The intronic rs5792235 variant is a potential causal variant in the region. It is likely that the region harbours multiple causal loci.
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