Melatonin ameliorates cardiac remodelling in fructose‑induced metabolic syndrome rat model by using genes encoding cardiac potassium ion channels
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CitationOvali, M. A., Oztopuz, O., & Vardar, S. A. (2021). Melatonin ameliorates cardiac remodelling in fructose-induced metabolic syndrome rat model by using genes encoding cardiac potassium ion channels. Molecular Biology Reports, 48(8), 5811–5819. https://doi.org/10.1007/s11033-021-06526-3
Background 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 efects 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 diferent 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 signifcantly 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 signifcantly 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 efects on ventricular repolarization by improving the prolonged QT duration in rats with metabolic syndrome and this efect was generated by the KCNQ and KCNH2 gene families.