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dc.contributor.authorAdams, Jeremy N
dc.contributor.authorMartelle, Susan E
dc.contributor.authorRaffield, Laura M
dc.contributor.authorFreedman, Barry I
dc.contributor.authorLangefeld, Carl D
dc.contributor.authorHsu, Fang-Chi
dc.contributor.authorMaldjian, Joseph A
dc.contributor.authorWilliamson, Jeff D
dc.contributor.authorHugenschmidt, Christina E
dc.contributor.authorCarr, J Jeffery
dc.contributor.authorCox, Amanda J
dc.contributor.authorBowden, Donald W
dc.date.accessioned2018-10-03T02:51:38Z
dc.date.available2018-10-03T02:51:38Z
dc.date.issued2016
dc.identifier.issn1056-8727
dc.identifier.doi10.1016/j.jdiacomp.2015.11.025
dc.identifier.urihttp://hdl.handle.net/10072/101927
dc.description.abstractAims—Human studies of links between advanced glycation end-products (AGEs) and disease phenotypes are less common than studies of animal and cell models. Here, we examined the association of total AGEs with diabetes risk factors in a predominately type 2 diabetes (T2D) affected cohort. Methods—AGEs were measured using an enzyme linked immunosorbant assay in 816 individuals from the DHS Mind Study (n=709 T2D affected), and association analyses were completed. Results—Total AGEs were associated with estimated glomerular filtration rate (p= 0.0054; β= −0.1291) and coronary artery calcification (p= 0.0352; β= 1.1489) in the entire cohort. No significant associations were observed when individuals with T2D were analyzed separately. In individuals without T2D, increased circulating AGEs were associated with increased BMI (p= 0.02, β = 0.138), low density lipoproteins (p=0.046, β = 17.07) and triglycerides (p= 0.0004, β = 0.125), and decreased carotid artery calcification (p= 0.0004, β = −1.2632) and estimated glomerular filtration rate (p= 0.0018, β = −0.1405). Strong trends were also observed for an association between AGEs and poorer cognitive performance on the digit symbol substitution test (p=0.046, β = −6.64) and decreased grey matter volume (p=0.037, β = −14.87). Conclusions—AGEs may play an important role in a number of phenotypes and diseases, although not necessarily in interindividual variation in people with T2D. Further evaluation of specific AGE molecules may shed more light on these relationships.
dc.description.peerreviewedYes
dc.languageEnglish
dc.language.isoeng
dc.publisherElsevier
dc.relation.ispartofpagefrom262
dc.relation.ispartofpageto268
dc.relation.ispartofissue2
dc.relation.ispartofjournalJournal of Diabetes and its Complications
dc.relation.ispartofvolume30
dc.subject.fieldofresearchClinical sciences
dc.subject.fieldofresearchClinical sciences not elsewhere classified
dc.subject.fieldofresearchcode3202
dc.subject.fieldofresearchcode320299
dc.titleAnalysis of Advanced Glycation End Products in the DHS Mind Study
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
dcterms.licensehttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.description.versionAccepted Manuscript (AM)
gro.rights.copyright© 2016 Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International Licence (http://creativecommons.org/licenses/by-nc-nd/4.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, providing that the work is properly cited.
gro.hasfulltextFull Text
gro.griffith.authorCox, Amanda J.


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