Lipoprotein(a)-activated immunity, insulin resistance and new-onset diabetes

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dc.contributor.authorKaya, Aysem
dc.contributor.authorOnat, Altan
dc.contributor.authorYuksel, Husniye
dc.contributor.authorCan, Gunay
dc.contributor.authorYuksel, Murat
dc.contributor.authorAdemoglu, Evin
dc.date.accessioned2024-04-24T16:24:19Z
dc.date.available2024-04-24T16:24:19Z
dc.date.issued2017
dc.departmentDicle Üniversitesien_US
dc.description.abstractObjectives: Some evidence suggests that serum lipoprotein[Lp](a) may be inversely linked to type-2 diabetes. We aimed to determine in nondiabetic people the relationship of serum [Lp](a) with insulin resistance and new-onset diabetes (NOD). Materials and methods: Population-based middle-aged adults (n = 1685) were categorized by fasting glucose and stratified to gender, having excluded prevalent diabetic subjects. NOD (n = 90) occurred over a median 5 years' follow-up. Results: Subjects that subsequently developed NOD, derived both from the normoglycemia and impaired fasting glucose (IFG) groups,were distinguished, among others, primarily by significantly elevated serum gamma glutamyltransferase, reduced Lp(a) (by 31%) and, compared to IFG, by low total cholesterol levels. Partial correlation of Lp(a) with homeostatic model assessment (HOMA) was inverse in normoglycemic men; such correlation, neutral in normoglycemic women, proved inverse in IFG (r = -0.17). Circulating Lp(a) in individuals with paired measures increased significantly (1.55-fold) in the period from baseline up to NOD. Multivariable-adjusted logistic regression analysis for NOD in combined sexes indicated independent and additive prediction by serum Lp(a), albeit inverse in direction (RR 0.84, [95%CI 0.72; 0.97]). Conclusion: Lp(a) is significantly reduced in the period preceding NOD and is inversely associated with HOMA index, observations consistent with underlying autoimmune activation.en_US
dc.description.sponsorshipTurkish Society of Cardiology, Istanbul; Turkish automotive company TOFAS, Istanbulen_US
dc.description.sponsorshipThe Turkish Society of Cardiology and the Turkish automotive company TOFAS, Istanbul, are acknowledged for support to the Turkish Adult Risk Factor study.en_US
dc.identifier.doi10.1080/00325481.2017.1342508
dc.identifier.endpage618en_US
dc.identifier.issn0032-5481
dc.identifier.issn1941-9260
dc.identifier.issue6en_US
dc.identifier.pmid28633585
dc.identifier.scopus2-s2.0-85021075461
dc.identifier.scopusqualityQ1
dc.identifier.startpage611en_US
dc.identifier.urihttps://doi.org/10.1080/00325481.2017.1342508
dc.identifier.urihttps://hdl.handle.net/11468/16654
dc.identifier.volume129en_US
dc.identifier.wosWOS:000406764700008
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherTaylor & Francis Ltden_US
dc.relation.ispartofPostgraduate Medicine
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAutoimmune Activationen_US
dc.subjectDiabetesen_US
dc.subjectType-2en_US
dc.subjectImpaired Fasting Glucoseen_US
dc.subjectInsulin Resistanceen_US
dc.subjectLipoprotein(A)en_US
dc.titleLipoprotein(a)-activated immunity, insulin resistance and new-onset diabetesen_US
dc.titleLipoprotein(a)-activated immunity, insulin resistance and new-onset diabetes
dc.typeArticleen_US

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