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PPAR Research
Volume 2016, Article ID 4518754, 10 pages
http://dx.doi.org/10.1155/2016/4518754
Research Article

Testosterone Replacement Modulates Cardiac Metabolic Remodeling after Myocardial Infarction by Upregulating PPARα

1Laboratory of Cardiovascular Internal Medicine Department, First Affiliated Hospital, Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin, Heilongjiang 150001, China
2Department of Emergency Surgery, First Affiliated Hospital, Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin, Heilongjiang 150001, China

Received 24 December 2015; Revised 17 April 2016; Accepted 24 May 2016

Academic Editor: Nigora Mukhamedova

Copyright © 2016 Jing Yang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Despite the importance of testosterone as a metabolic hormone, its effects on myocardial metabolism in the ischemic heart remain unclear. Myocardial ischemia leads to metabolic remodeling, ultimately resulting in ATP deficiency and cardiac dysfunction. In the present study, the effects of testosterone replacement on the ischemic heart were assessed in a castrated rat myocardial infarction model established by ligating the left anterior descending coronary artery 2 weeks after castration. The results of real-time PCR and Western blot analyses showed that peroxisome proliferator-activated receptor α (PPARα) decreased in the ischemic myocardium of castrated rats, compared with the sham-castration group, and the mRNA expression of genes involved in fatty acid metabolism (the fatty acid translocase CD36, carnitine palmitoyltransferase I, and medium-chain acyl-CoA dehydrogenase) and glucose transporter-4 also decreased. A decline in ATP levels in the castrated rats was accompanied by increased cardiomyocyte apoptosis and fibrosis and impaired cardiac function, compared with the sham-castration group, and these detrimental effects were reversed by testosterone replacement. Taken together, our findings suggest that testosterone can modulate myocardial metabolic remodeling by upregulating PPARα after myocardial infarction, exerting a protective effect on cardiac function.