Insulin response to oral glucose loading and coronary artery disease in nondiabetics

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dc.contributor.authorKarabulut, A
dc.contributor.authorIltumur, K
dc.contributor.authorToprak, N
dc.contributor.authorTuzcu, AK
dc.contributor.authorKara, IH
dc.contributor.authorKaplan, A
dc.contributor.authorAksu, Y
dc.date.accessioned2024-04-24T17:18:04Z
dc.date.available2024-04-24T17:18:04Z
dc.date.issued2005
dc.departmentDicle Üniversitesien_US
dc.description.abstractHyperinsulinemia is related to coronary artery disease (CAD), as an indication of decreased insulin sensitivity. Although there are man), Studies showing the relation between fasting insulin levels and insulin resistance. there are fewer studies on postprandial insulin levels. The aim of the present Study was to investigate the relationship between postprandial insulin levels and CAD and its extent in our patients. For this purpose, oral glucose tolerance testing was performed in 222 patients with no known diabetes and who were scheduled to undergo diagnostic coronary angiography. The patients were first separated into two groups, one group (group I) having an insulin response within reference values to oral glucose loading, and the other group (group II) with a higher than normal insulin response. The presence and extent of CAD in the two groups were compared. While 65% of the patients in group I had CAD, this rate increased to 79% in group 2 patients (P = 0.02). The mean vessel scores were 0.92 +/- 0.78 in group I and 1.67 +/- 0.99 (P < 0.0001) in group 2 patients. The stenosis scores were 2.192 +/- 2.077 in group I and 5.588 +/- 3.519 (P < 0.001) in group 2, while the extent scores were 1.230 +/- 1.292 in group I and 2.729 +/- 1.847 in group 2 (P < 0.0001). The differences between the two groups were significant. Postprandial insulin values were positively correlated with CAD (P = 0.001, r = 0.214), vessel scores (P < 0.0001, r = 0.326), stenosis scores (P < 0.0001. r = 0.261), and extent scores (P < 0.0001, r = 0.419). Logistic regression analysis revealed hyperinsulinemia increased CAD independent from the other risk factors (OR = 5.742 CI 95%: 1.809-18.227, P = 0.003).en_US
dc.identifier.doi10.1536/ihj.46.761
dc.identifier.endpage770en_US
dc.identifier.issn1349-2365
dc.identifier.issn1349-3299
dc.identifier.issue5en_US
dc.identifier.pmid16272767
dc.identifier.scopus2-s2.0-33644873630
dc.identifier.scopusqualityQ3
dc.identifier.startpage761en_US
dc.identifier.urihttps://doi.org/10.1536/ihj.46.761
dc.identifier.urihttps://hdl.handle.net/11468/18579
dc.identifier.volume46en_US
dc.identifier.wosWOS:000233880500001
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherInt Heart Journal Assocen_US
dc.relation.ispartofInternational Heart Journal
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectPostprandial Hyperinsulinemiaen_US
dc.subjectSeverity Of Coronary Artery Diseaseen_US
dc.titleInsulin response to oral glucose loading and coronary artery disease in nondiabeticsen_US
dc.titleInsulin response to oral glucose loading and coronary artery disease in nondiabetics
dc.typeArticleen_US

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