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Article: Advanced glycation end products and endothelial dysfunction in type 2 diabetes

TitleAdvanced glycation end products and endothelial dysfunction in type 2 diabetes
Authors
Issue Date2002
PublisherAmerican Diabetes Association. The Journal's web site is located at http://diabetes.diabetesjournals.org/
Citation
Diabetes Care, 2002, v. 25 n. 6, p. 1055-1059 How to Cite?
AbstractOBJECTIVE - Data from experimental studies have suggested that the increased formation of advanced glycation end products (AGEs) is one of the causes of endothelial dysfunction in diabetes. This study was performed to investigate whether changes in endothelium-dependent vasodilation, a marker of endothelial function, were related to serum AGEs concentrations in patients with type 2 diabetes. RESEARCH DESIGN AND METHODS - For this study, 170 patients with type 2 diabetes and 83 healthy nondiabetic control subjects of similar age were recruited. Serum AGEs were assayed by competitive enzyme-linked immunosorbent assay. Endothelium-dependent and -independent vasodilation of the brachial artery was measured by high-resolution vascular ultrasound. RESULTS - Serum AGEs were increased in diabetic patients compared with control subjects (4.6 ± 0.7 vs. 3.1 ± 0.8 unit/ml; P < 0.01), and both endothelium-dependent (5.1 ± 2.5 vs. 9.1 ± 4.1%; P < 0.01) and endothelium-independent vasodilation (13.2 ± 4.6 vs. 16.4 ± 5.5%; P < 0.01) were impaired. On univariate analysis of all subjects, serum AGEs correlated with endothelium-dependent vasodilation (r = -0.51, P < 0.01); a weaker association was found with endothelium-independent vasodilation (r = -0.24, P < 0.01). On multiple regression analyses including age, sex, smoking status, and plasma lipids, only serum AGEs remained a significant independent determinant of endothelium-dependent vasodilation (r2 = 0.34, P < 0.01). CONCLUSIONS - Increased serum concentrations of AGEs in patients with type 2 diabetes is associated with endothelial dysfunction, independent of other cardiovascular risk factors. Further studies to determine whether treatment targeting AGEs will lead to an amelioration of endothelial dysfunction are warranted.
Persistent Identifierhttp://hdl.handle.net/10722/162621
ISSN
2015 Impact Factor: 8.934
2015 SCImago Journal Rankings: 5.827
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTan, KCBen_US
dc.contributor.authorChow, WSen_US
dc.contributor.authorAi, VHGen_US
dc.contributor.authorMetz, Cen_US
dc.contributor.authorBucala, Ren_US
dc.contributor.authorLam, KSLen_US
dc.date.accessioned2012-09-05T05:21:44Z-
dc.date.available2012-09-05T05:21:44Z-
dc.date.issued2002en_US
dc.identifier.citationDiabetes Care, 2002, v. 25 n. 6, p. 1055-1059en_US
dc.identifier.issn0149-5992en_US
dc.identifier.urihttp://hdl.handle.net/10722/162621-
dc.description.abstractOBJECTIVE - Data from experimental studies have suggested that the increased formation of advanced glycation end products (AGEs) is one of the causes of endothelial dysfunction in diabetes. This study was performed to investigate whether changes in endothelium-dependent vasodilation, a marker of endothelial function, were related to serum AGEs concentrations in patients with type 2 diabetes. RESEARCH DESIGN AND METHODS - For this study, 170 patients with type 2 diabetes and 83 healthy nondiabetic control subjects of similar age were recruited. Serum AGEs were assayed by competitive enzyme-linked immunosorbent assay. Endothelium-dependent and -independent vasodilation of the brachial artery was measured by high-resolution vascular ultrasound. RESULTS - Serum AGEs were increased in diabetic patients compared with control subjects (4.6 ± 0.7 vs. 3.1 ± 0.8 unit/ml; P < 0.01), and both endothelium-dependent (5.1 ± 2.5 vs. 9.1 ± 4.1%; P < 0.01) and endothelium-independent vasodilation (13.2 ± 4.6 vs. 16.4 ± 5.5%; P < 0.01) were impaired. On univariate analysis of all subjects, serum AGEs correlated with endothelium-dependent vasodilation (r = -0.51, P < 0.01); a weaker association was found with endothelium-independent vasodilation (r = -0.24, P < 0.01). On multiple regression analyses including age, sex, smoking status, and plasma lipids, only serum AGEs remained a significant independent determinant of endothelium-dependent vasodilation (r2 = 0.34, P < 0.01). CONCLUSIONS - Increased serum concentrations of AGEs in patients with type 2 diabetes is associated with endothelial dysfunction, independent of other cardiovascular risk factors. Further studies to determine whether treatment targeting AGEs will lead to an amelioration of endothelial dysfunction are warranted.en_US
dc.languageengen_US
dc.publisherAmerican Diabetes Association. The Journal's web site is located at http://diabetes.diabetesjournals.org/en_US
dc.relation.ispartofDiabetes Careen_US
dc.subject.meshAge Of Onseten_US
dc.subject.meshBiological Markers - Blooden_US
dc.subject.meshBlood Pressureen_US
dc.subject.meshCholesterol - Blooden_US
dc.subject.meshDiabetes Mellitus, Type 2 - Blood - Physiopathologyen_US
dc.subject.meshEndothelium, Vascular - Physiology - Physiopathologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshGlycosylation End Products, Advanced - Blooden_US
dc.subject.meshHumansen_US
dc.subject.meshLipoproteins, Hdl - Blooden_US
dc.subject.meshLipoproteins, Ldl - Blooden_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshReference Valuesen_US
dc.subject.meshRegression Analysisen_US
dc.subject.meshSmokingen_US
dc.subject.meshTriglycerides - Blooden_US
dc.subject.meshVasodilation - Physiologyen_US
dc.titleAdvanced glycation end products and endothelial dysfunction in type 2 diabetesen_US
dc.typeArticleen_US
dc.identifier.emailTan, KCB:kcbtan@hku.hken_US
dc.identifier.emailLam, KSL:ksllam@hku.hken_US
dc.identifier.authorityTan, KCB=rp00402en_US
dc.identifier.authorityLam, KSL=rp00343en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.2337/diacare.25.6.1055en_US
dc.identifier.pmid12032114-
dc.identifier.scopuseid_2-s2.0-0036599334en_US
dc.identifier.hkuros77991-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036599334&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume25en_US
dc.identifier.issue6en_US
dc.identifier.spage1055en_US
dc.identifier.epage1059en_US
dc.identifier.isiWOS:000185503800018-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridTan, KCB=8082703100en_US
dc.identifier.scopusauthoridChow, WS=7402281153en_US
dc.identifier.scopusauthoridAi, VHG=6603342063en_US
dc.identifier.scopusauthoridMetz, C=7102876220en_US
dc.identifier.scopusauthoridBucala, R=7102379822en_US
dc.identifier.scopusauthoridLam, KSL=8082870600en_US

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