کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6312778 | 1619036 | 2016 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Air pollution and diabetes association: Modification by type 2 diabetes genetic risk score
ترجمه فارسی عنوان
آلودگی هوا و دیابت: اصلاح با نمره خطر ابتلا به دیابت نوع 2
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کلمات کلیدی
HWESAPALDIAT1DHbA1cIPWGRsT2DGEIRAFBCFMAFPM10CNGPM2.5DNA - DNA یا اسید دزوکسی ریبونوکلئیکEDTA - اتیلن دی آمین تترا استیک اسید Ethylenediaminetetraacetic acid - اتیلینیدامین تتراستیک اسیدdeoxyribonucleic acid - اسید deoxyribonucleicHardy-Weinberg equilibrium - تعادل هاردی-وینبرگgene-environment interaction - تعامل ژن و محیط زیستgene-environment interactions - تعاملات ژن-محیطیDiabetes mellitus - دیابت قندیType 2 diabetes - دیابت نوع 2Type 1 diabetes - دیابت نوع۱particulate matter - ذرات معلقbody mass index - شاخص توده بدنBMI - شاخص توده بدنیBeta cell function - عملکرد سلول بتاconfidence interval - فاصله اطمینانminor allele frequency - فراوانی آللی جزئیGenome-wide association studies - مطالعات مرتبط با ژنومGWAS - مطالعهٔ همخوانی سراسر ژنومInsulin resistance - مقاومت به انسولینodds ratio - نسبت شانس هاgenetic risk score - نمره خطر ژنتیکیglycosylated haemoglobin - هموگلوبین گلیکوزیله شدهinverse probability weighting - وزن احتمال معکوسSingle nucleotide polymorphism - پلیمورفیسم تک نوکلئوتیدیSNP - چندریختی تک-نوکلئوتید
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
شیمی زیست محیطی
چکیده انگلیسی
Exposure to ambient air pollution (AP) exposure has been linked to type 2 diabetes (T2D) risk. Evidence on the impact of T2D genetic variants on AP susceptibility is lacking. Compared to single variants, joint genetic variants contribute substantially to disease risk. We investigated the modification of AP and diabetes association by a genetic risk score (GRS) covering 63 T2D genes in 1524 first follow-up participants of the Swiss cohort study on air pollution and lung and heart diseases in adults. Genome-wide data and covariates were available from a nested asthma case-control study design. AP was estimated as 10-year mean residential particulate matter < 10 μm (PM10). We computed count-GRS and weighted-GRS, and applied PM10 interaction terms in mixed logistic regressions, on odds of diabetes. Analyses were stratified by pathways of diabetes pathology and by asthma status. Diabetes prevalence was 4.6% and mean exposure to PM10 was 22 μg/m3. Odds of diabetes increased by 8% (95% confidence interval: 2, 14%) per T2D risk allele and by 35% (â 8, 97%) per 10 μg/m3 exposure to PM10. We observed a positive interaction between PM10 and count-GRS on diabetes [ORinteraction = 1.10 (1.01, 1.20)], associations being strongest among participants at the highest quartile of count-GRS [OR: 1.97 (1.00, 3.87)]. Stronger interactions were observed with variants of the GRS involved in insulin resistance [(ORinteraction = 1.22 (1.00, 1.50)] than with variants related to beta-cell function. Interactions with count-GRS were stronger among asthma cases. We observed similar results with weighted-GRS. Five single variants near GRB14, UBE2E2, PTPRD, VPS26A and KCNQ1 showed nominally significant interactions with PM10 (P < 0.05). Our results suggest that genetic risk for T2D may modify susceptibility to air pollution through alterations in insulin sensitivity. These results need confirmation in diabetes cohort consortia.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Environment International - Volume 94, September 2016, Pages 263-271
Journal: Environment International - Volume 94, September 2016, Pages 263-271
نویسندگان
Ikenna C. Eze, Medea Imboden, Ashish Kumar, Arnold von Eckardstein, Daiana Stolz, Margaret W. Gerbase, Nino Künzli, Marco Pons, Florian Kronenberg, Christian Schindler, Nicole Probst-Hensch,