Melatonin ameliorates cardiac remodelling in fructose-induced metabolic syndrome rat model by using genes encoding cardiac potassium ion channels

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dc.authoridOztopuz, Rahime Ozlem/0000-0002-1373-6311
dc.authoridOvali, Mehmet Akif/0000-0002-3672-871X
dc.authorwosidOztopuz, Rahime Ozlem/AFK-7508-2022
dc.contributor.authorOvali, Mehmet Akif
dc.contributor.authorOztopuz, Ozlem
dc.contributor.authorVardar, Selma Arzu
dc.date.accessioned2024-06-12T11:08:14Z
dc.date.available2024-06-12T11:08:14Z
dc.date.issued2021
dc.departmentTrakya Üniversitesien_US
dc.description.abstractBackground Metabolic syndrome comprises a group of disorders, including cardiac abnormalities. Ventricular arrhythmias observed in metabolic syndrome are due to the impaired ventricular repolarization. This study aims to determine the effects of melatonin on cardiac ventricular repolarization in metabolic syndrome rat model. Methods and results Sprague-Dawley rats were divided into control (n = 8), melatonin (n = 8), metabolic syndrome (n = 8) and metabolic syndrome + melatonin (n = 8) groups. Fructose (200 g/lt/day) was added into the drinking water during 8 weeks of rats to induce metabolic syndrome model. In the last two weeks, melatonin (20 mg/kg/day) was administered via oral gavage. Blood pressure measurements and ECG recordings were taken at three different times. Blood and left ventricular tissue samples were harvested and the KCNQ1,3 and KCNH2 gene expressions were analysed by qRT-PCR method. We observed insulin resistance, hyperglycemia, dyslipidemia and higher systolic blood pressure in metabolic syndrome group (p < 0.01, for all). Prolonged QT interval was observed in metabolic syndrome group (p < 0.001). The expression levels of the KCNQ genes encoding the Kv7 channel was significantly reduced, however KCNH2 gene which encodes Kv11.1 channel was increased in metabolic syndrome group compared to control group (p < 0.05, p < 0.001, respectively). Melatonin significantly normalised the prolongation on QT interval in metabolic syndrome group (p < 0.001) and the expressions of the KCNQ (p < 0.002) and KCNH2 genes (p = 0.003). Conclusions The present study revealed that melatonin had ameliorative effects on ventricular repolarization by improving the prolonged QT duration in rats with metabolic syndrome and this effect was generated by the KCNQ and KCNH2 gene families.en_US
dc.description.sponsorshipfoundation of TUBAP (Scientific Research Projects Office of Trakya University) [TUBAP 2018/291]en_US
dc.description.sponsorshipThis study is supported by the foundation of TUBAP (Scientific Research Projects Office of Trakya University, Project number: TUBAP 2018/291) and summarised from PhD Thesis of the Corresponding Author.en_US
dc.identifier.doi10.1007/s11033-021-06526-3
dc.identifier.endpage5819en_US
dc.identifier.issn0301-4851
dc.identifier.issn1573-4978
dc.identifier.issue8en_US
dc.identifier.pmid34347240en_US
dc.identifier.scopus2-s2.0-85111723569en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage5811en_US
dc.identifier.urihttps://doi.org/10.1007/s11033-021-06526-3
dc.identifier.urihttps://hdl.handle.net/20.500.14551/22363
dc.identifier.volume48en_US
dc.identifier.wosWOS:000681163800003en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpringeren_US
dc.relation.ispartofMolecular Biology Reportsen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectMelatoninen_US
dc.subjectMetabolic Syndromeen_US
dc.subjectFructoseen_US
dc.subjectCardiac Ions Channelsen_US
dc.subjectQtcen_US
dc.subjectLong-Qt Syndromeen_US
dc.subjectMtnr1ben_US
dc.subjectKcnqen_US
dc.titleMelatonin ameliorates cardiac remodelling in fructose-induced metabolic syndrome rat model by using genes encoding cardiac potassium ion channelsen_US
dc.typeArticleen_US

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