Activated AMPK attenuates cardiac hypertrophy in rats through increasing myocardial fatty acid oxidation |
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| Authors: | YIN Ran DONG Yu-gang LI Hong-liang LIU Dan |
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| Institution: | 1.Department of Cardiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, China;2.Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing 100005, China. E-mail： ygdong@medmail.com.cn |
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| Abstract: | AIM: To investigate the antihypertrophic function of adenosine monophosphate-activated protein kinase(AMPK) and its effects on myocardial fatty acid oxidation.METHODS: The model of cardiac hypertrophy was produced by banding abdominal aorta (transaortic constriction, TAC) in male Sprague-Dawley rats. 5-aminoimidazole-4-carboxamide ribonucleoside(AICAR), a pharmacological activator of AMPK, was injected subcutaneously (0.5 mg·kg-1·d-1) 24 hours after operation and continued till 7 weeks after operation. Echocardiographic and ventricular remodeling parameters, free fatty acid concentration in blood serum and myocardium, and expression of peroxisome proliferator-activated receptor(PPARα) and carnitine palmityl transferase(CPT-I) mRNA were investigated after treatment of AICAR or vehicle for 7 weeks. RESULTS: Compared with control group, treatment of rats subjected to TAC with AICAR significantly increased the mRNA expression of PPARα and CPT-I and subsequently decreased free fatty acid concentration in blood and myocardium, improved echocardiographic characteristics, and reduced the increases in the heart weight/body weight ratio and myocyte diameter.CONCLUSION: Pharmacological activation of AMPK may attenuate cardiac hypertrophy through increasing myocardial fatty acid oxidation. |
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| Keywords: | Adenosine monophosphate-activated protein kinase Cardiac hypertrophy Fatty acid oxidation Mitochondria |
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