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More importantly, we aimed to identify the potential effects of melatonin on cardiac metabolic reprogramming and energetics in doxorubicin\u2010induced heart failure. Male Wistar rats (<jats:italic>n<\/jats:italic>\u2009=\u200918) were randomly divided into three groups (<jats:italic>n<\/jats:italic>\u2009=\u20096\/group) to receive either (1) normal saline solution as a control, (2) 3\u2009mg\/kg\/day of doxorubicin on Days 0, 4, 8, 15, 22, and 29, or (3) 3\u2009mg\/kg\/day of doxorubicin on Days 0, 4, 8, 15, 22, and 29 plus 10\u2009mg\/kg\/day of melatonin on Days 0\u201329. On Day 30, echocardiography was carried out and heart rate variability was analyzed for the evaluation of cardiac function. The rats were euthanized on the following day to enable the collection of ventricular cardiac tissue. Compared to the control group, the hearts of rats treated with doxorubicin alone exhibited impaired cardiac function, increased glucose and ketone body utilization, decreased fat utilization, decreased succinate oxidation, and decreased production of adenosine triphosphate. The cotreatment with melatonin could restore cardiac function, glucose and ketone body utilization, and adenosine triphosphate production in the heart. Interestingly, the cotreatment with melatonin led to an increase in cardiac fatty acid oxidation, branched\u2010chain amino acid catabolism, and anaplerosis. All of these findings highlighted the potential efficacy of melatonin with regard to cardiac metabolic reprogramming and energetics. Our findings also suggested that melatonin could be considered as an adjunctive treatment for doxorubicin\u2010induced heart failure in clinical practice.<\/jats:p>","DOI":"10.1111\/jpi.12884","type":"journal-article","created":{"date-parts":[[2023,5,13]],"date-time":"2023-05-13T07:40:06Z","timestamp":1683963606000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Effects of melatonin on cardiac metabolic reprogramming in doxorubicin\u2010induced heart failure rats: A metabolomics study for potential therapeutic targets"],"prefix":"10.1111","volume":"75","author":[{"given":"Chanisa","family":"Thonusin","sequence":"first","affiliation":[{"name":"Cardiac Electrophysiology Unit, Department of Physiology Chiang Mai University  Chiang Mai Thailand"},{"name":"Cardiac Electrophysiology Research and Training Center, Faculty of Medicine Chiang Mai University  Chiang Mai Thailand"},{"name":"Center of Excellence in Cardiac 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