| Chronic melatonin consumption prevents obesity-related metabolic abnormalities and protects the heart against myocardial ischemia and reperfusion injury in a prediabetic model of diet-induced obesity. | |
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MedLine Citation:
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PMID: 21073520 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Obesity, a major risk factor for ischemic heart disease, is associated with increased oxidative stress and reduced antioxidant status. Melatonin, a potent free radical scavenger and antioxidant, has powerful cardioprotective effects in lean animals but its efficacy in obesity is unknown. We investigated the effects of chronic melatonin administration on the development of the metabolic syndrome as well as ischemia-reperfusion injury in a rat model of diet-induced obesity (DIO). Male Wistar rats received a control diet, a control diet with melatonin, a high-calorie diet, or a high-calorie diet with melatonin (DM). Melatonin (4 mg/kg/day) was administered in the drinking water. After 16 wk, biometric and blood metabolic parameters were measured. Hearts were perfused ex vivo for the evaluation of myocardial function, infarct size (IFS) and biochemical changes [activation of PKB/Akt, ERK, p38 MAPK, AMPK, and glucose transporter (GLUT)-4 expression). The high-calorie diet caused increases in body weight (BW), visceral adiposity, serum insulin and triglycerides (TRIG), with no change in glucose levels. Melatonin treatment reduced the BW gain, visceral adiposity, blood TRIG, serum insulin, homeostatic model assessment index and thiobarbituric acid reactive substances in the DIO group. Melatonin reduced IFS in DIO and control groups and increased percentage recovery of functional performance of DIO hearts. During reperfusion, hearts from melatonin-treated rats had increased activation of PKB/Akt, ERK42/44 and reduced p38 MAPK activation. Chronic melatonin treatment prevented the metabolic abnormalities induced by DIO and protected the heart against ischemia-reperfusion injury. These beneficial effects were associated with activation of the reperfusion injury salvage kinases pathway. |
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Authors:
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Frederic Nduhirabandi; Eugene F Du Toit; Dee Blackhurst; David Marais; Amanda Lochner |
Publication Detail:
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Type: JOURNAL ARTICLE Date: 2010-11-15 |
Journal Detail:
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Title: Journal of pineal research Volume: - ISSN: 1600-079X ISO Abbreviation: J. Pineal Res. Publication Date: 2010 Nov |
Date Detail:
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Created Date: 2010-11-15 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8504412 Medline TA: J Pineal Res Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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© 2010 The Authors. Journal of Pineal Research © 2010 John Wiley & Sons A/S. |
Affiliation:
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Division of Medical Physiology, Department of Biomedical Sciences, Faculty of Health Sciences, Stellenbosch University, Stellenbosch, South Africa School of Medical Science, Griffith University, Australia Division of Lipidology, Department of Internal Medicine, University of Cape Town, Cape Town, South Africa. |
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