Irisin: A potentially candidate marker for myocardial infarction

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dc.contributor.authorKuloglu, Tuncay
dc.contributor.authorAydin, Suna
dc.contributor.authorEren, Mehmet Nesimi
dc.contributor.authorYilmaz, Musa
dc.contributor.authorSahin, Ibrahim
dc.contributor.authorKalayci, Mehmet
dc.contributor.authorSarman, Emine
dc.date.accessioned2024-04-24T16:15:48Z
dc.date.available2024-04-24T16:15:48Z
dc.date.issued2014
dc.departmentDicle Üniversitesien_US
dc.description.abstractMyocardial infarction (MI) causes energy depletion through imbalance between coronary blood supply and myocardial demand. Irisin produced by the heart reduces ATP production by increasing heat generation. Energy depletion affects irisin concentration in circulation and cardiac tissues, suggesting an association with MI. We examined: (1) irisin expression immunohistochemically in rat heart, skeletal muscle, kidney and liver in isoproterenol (ISO)-induced MI, and (2) serum irisin concentration by ELISA. Rats were randomly allocated into 6 groups (n=6), (i) control, (ii) ISO (1 h), (iii) ISO (2 h), (iv) ISO (4 h), (v) ISO (6 h), and (vi) ISO (24 h), 200 mg ISO in each case. Rats were decapitated and the blood and tissues collected for irisin analysis. Blood was centrifuged at 1792 g for 5 min. Tissues were washed with saline and fixed in 10% formalin for histology. Serum irisin levels gradually decreased from 1 h to 24h in MI rats compared with controls, the minimum being at 2 h, increasing again after 6 h. Cardiac muscle cells, glomerular, peritubular renal cortical interstitial cells, hepatocytes and liver sinusoidal cells and perimysium, endomysium and nucleoi of skeletal muscle were irisin positive, but its synthesis decreased 1-4 h after MI. At all time-points, irisin increased near myocardial connective tissue, with production in skeletal muscle, liver and kidney recovering after 6 h, although slower than controls. Unique insight into the pathogenesis of MI is shown, and the gradually decrease of serum irisin might be a diagnostic marker for MI. (C) 2014 Elsevier Inc. All rights reserved.en_US
dc.identifier.doi10.1016/j.peptides.2014.02.008
dc.identifier.endpage91en_US
dc.identifier.issn0196-9781
dc.identifier.issn1873-5169
dc.identifier.pmid24576483
dc.identifier.scopus2-s2.0-84896140402
dc.identifier.scopusqualityQ2
dc.identifier.startpage85en_US
dc.identifier.urihttps://doi.org/10.1016/j.peptides.2014.02.008
dc.identifier.urihttps://hdl.handle.net/11468/15931
dc.identifier.volume55en_US
dc.identifier.wosWOS:000335503900012
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherElsevier Science Incen_US
dc.relation.ispartofPeptides
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectIrisinen_US
dc.subjectMyocardial Infarctionen_US
dc.subjectIsoproterenolen_US
dc.subjectHearten_US
dc.subjectSkeletal Muscleen_US
dc.subjectKidneysen_US
dc.titleIrisin: A potentially candidate marker for myocardial infarctionen_US
dc.titleIrisin: A potentially candidate marker for myocardial infarction
dc.typeArticleen_US

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