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Lack of interaction of beta-cell-function-associated variants with hypertension on change in fasting glucose and diabetes risk: the Framingham Offspring Study

dc.contributor.authorMiguel Yanes, José María De
dc.contributor.authorPorneala, Bianca
dc.contributor.authorPencina, Michael
dc.contributor.authorFox, Caroline
dc.contributor.authorFlorez, Jose
dc.contributor.authorSiscovick, David
dc.contributor.authorDupuis, Josée
dc.contributor.authorMeigs, James
dc.date.accessioned2024-01-12T09:19:23Z
dc.date.available2024-01-12T09:19:23Z
dc.date.issued2013
dc.description.abstractObjective: To test whether pancreatic beta-cell genetic frailty and hypertension (HTN) interact in their associations with change over time in fasting glucose (ΔFG) or type 2 diabetes mellitus (T2D) risk. Methods and results: We pooled data from 3471 Framingham Offspring Study participants into six ∼4-year periods (15 852 person-examinations; mean age 52; 54% women). We defined two genetic exposures reflecting beta-cell genetic risk burden: single nucleotide polymorphism (SNP) score counts of fasting glucose-associated and T2D-associated risk alleles at 16 and 33 putative beta-cell loci, respectively; and three HTN exposures: HTN versus no-HTN; treated versus untreated HTN; and five mutually exclusive antihypertensive categories (beta-blockers, thiazides, renin-angiotensin system agents, combinations, others) versus untreated HTN. We tested ∼4-year mean ΔFG or odds of T2D by per-risk allele score change and HTN category, seeking genetic score-by-HTN interaction. Genetic scores increased ∼4-year ΔFG (0.6 mg/dl per-risk allele; P = 8.9 × 10(-16)) and T2D-risk (∼17% per-risk allele; P = 2.1 × 10(-7)). As compared to no-HTN, HTN conferred higher ΔFG (2.6 versus 1.7 mg/dl; P < 0.0001) and T2D-risk [odds ratio (OR) = 2.9, 95% confidence interval (CI) 2.8-3.0; P < 0.0001]. As compared to untreated HTN, treated HTN conferred higher ΔFG (3.4 versus 3.0 mg/dl; P < 0.0001) and T2D-risk (OR = 1.4, 95% CI 1.3-1.5; P = 0.02). Beta-blockers (OR = 1.6, 95% CI 1.1-2.4), combinations (OR = 1.6, 95% CI 1.1-2.5), and others (OR = 2.0, 95% CI 1.4-2.9) increased T2D-risk (all P < 0.02). In joint models including interaction terms, all genetic score-by-HTN interaction terms were P value greater than 0.05. In joint models without interaction, fasting glucose-SNP or T2D-SNP genetic scores (both P < 0.001) and HTN (P < 0.0001) independently increased ΔFG or T2D-risk. Conclusion: HTN, HTN treatment, and common fasting glucose-SNP genetic score/T2D-SNP genetic score independently predicted ΔFG and T2D incidence, but did not modify each other's association with ΔFG or T2D risk.
dc.description.departmentDepto. de Medicina
dc.description.facultyFac. de Medicina
dc.description.refereedTRUE
dc.description.sponsorshipNational Institute for Diabetes and Digestive and Kidney Diseases
dc.description.sponsorshipNational Institutes of Health
dc.description.sponsorshipBoston University School of Medicine
dc.description.sponsorshipSNP Health Association Resource
dc.description.sponsorshipAffimetrix
dc.description.sponsorshipBoston Medical Center
dc.description.statuspub
dc.identifier.citationde Miguel-Yanes JM, Porneala B, Pencina MJ, Fox CS, Florez JC, Siscovick DS, Dupuis J, Meigs JB. Lack of interaction of beta-cell-function-associated variants with hypertension on change in fasting glucose and diabetes risk: the Framingham Offspring Study. J Hypertens. 2013 May;31(5):1001-9
dc.identifier.doi10.1097/HJH.0b013e32835f5a83
dc.identifier.issn0263-6352
dc.identifier.officialurlhtttps://doi.org/10.1097/HJH.0b013e32835f5a83
dc.identifier.relatedurlhttps://pubmed.ncbi.nlm.nih.gov/23425704/
dc.identifier.urihttps://hdl.handle.net/20.500.14352/92681
dc.issue.number5
dc.journal.titleJournal of Hypertension
dc.language.isoeng
dc.page.final1009
dc.page.initial1001
dc.publisherLippincott, Williams & Wilkins
dc.rights.accessRightsrestricted access
dc.subject.cdu616.1/.9
dc.subject.keywordFasting glucose
dc.subject.keywordFramingham
dc.subject.keywordGenes
dc.subject.keywordGenetic risk scores
dc.subject.keywordHypertension
dc.subject.keywordHypertension treatment
dc.subject.ucmMedicina interna
dc.subject.unesco3205 Medicina Interna
dc.titleLack of interaction of beta-cell-function-associated variants with hypertension on change in fasting glucose and diabetes risk: the Framingham Offspring Study
dc.typejournal article
dc.type.hasVersionVoR
dc.volume.number31
dspace.entity.typePublication
relation.isAuthorOfPublication7ed9b0a8-df93-404b-b68b-876caee32ec8
relation.isAuthorOfPublication.latestForDiscovery7ed9b0a8-df93-404b-b68b-876caee32ec8

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