Effect of AMPK on Energy Metabolism of Mice in Exercise-induced and Pathological Cardiac Hypertrophy

To explore the differences of energy metabolism in exercise-induced and pathological cardiac hypertrophy and its regulation factor.Methods:The exercise-induced cardiac hypertrophy model was made by swim training, and the pathological model was made by transverse aortic constriction (TAC) .12-week-old C57Bl/6J mice were divided randomly into control group, swim group, sham group and TAC group.By the end of experiments, cardiac hypertrophy, contractility were evaluated by echocardiography, and myocardial fibrosis were detected by Masson staining.Myocardial free fatty acid (FFA) and glucose levels were measured by colorimetric detection, AMPK and PPAR-αmRNA expression were detected by real time PCR (RTPCR) .Results:1) Significant cardiac hypertrophy could both produced by swim training and TAC in mice.Compared with corresponding control groups, interventricular septum thickness (IVS) and left ventricular posterior wall thickness (LVPW) of two cardiac hypertrophy models were significantly increased (P<0.05) , heart weight/body weight ratio, left ventricular weight/tibia length ratio were also increased significantly (P<0.05) compared with corresponding control groups.ANP and BNP mRNA expression of TAC group were higher than those of swim group obviously (P<0.01) , and its' myocardial fibrosis was significantly heavier than swim group.2) FFA in myocardium of TAC group were significantly increased compared with those of sham (P<0.05) and swim group (P<0.01) , Glu in myocardial of swim group were significantly higher than those of control (P<0.05) and TAC group (P<0.05) . (3) AMPK mRNA expression levels were significantly increased of swim group compared with93control (P<0.05) and TAC group (P<0.01) , while PPAR-αmRNA expression levels of TAC group were significantly lower than those of sham (P<0.05) and swim group (P<0.05) .Conclusion:Exercise could improve energy metabolism in cardiac hypertrophy, and reduce energy metabolism embryonic recapitulation through activating of AMPK expression.