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In addition, increased numbers of autophagic vacuoles and lysosomes were accompanied increased AMP-activated protein kinase activity and suppression of mammalian target of rapamycin phosphorylation. Chronic metformin therapy restores cardiac AMPK activity and improves cardiac function in diabetic OVE26 mice, supporting that dysregulation of AMPK is an important event in the pathogenesis of diabetic cardiomyopathy.Elucidating the mechanism responsible for the decreased AMPK activity in the diabetic heart may open a new horizon for the treatment and prevention of diabetic cardiomyopathy. Plasma insulin and HbA1c were each measured using blood collected from the carotid artery after catheterization. Name must be less than 100 characters ), Gifu University Graduate School of Medicine, JapanDepartment of Cardiology (H.K., G.N., A.Y., S.M., T.W., T.K., Y.Y., A.M., M.K., G.T., S.M. However, echocardiography and cardiac catheterization revealed an enlarged LV cavity and impaired LV function in 36-week-old SgcdMetabolic defects have been noted in dystrophic, β-sarcoglycan-null mice.Electron microscopy revealed severe degeneration within cardiomyocytes from SgcdMyocardial expression of myosin heavy chain, troponin I, and GATA-4 was significantly reduced in SgcdDouble immunofluorescent labeling revealed that the numbers of LC3-positive autophagic vacuoles were significantly greater within cardiomyocytes from SgcdWe observed a significant increase in the level of activated AMPK (p-AMPK/AMPK) in SgcdDirect ATP measurement revealed that the myocardial ATP content was significantly lower in SgcdFinally, we investigated the effect of metformin on skeletal muscles using quadriceps and diaphragm muscles (Figures III and IV in the We found that metformin treatment improved cardiac function and remodeling in sarcoglycanopathy-associated DCM, with no major side effects. In addition to lowering blood glucose levels, metformin exerts pleiotropic effects involving AMP-activated protein kinase in cardiovascular disease. This site needs JavaScript to work properly. Homogenates were centrifuged at 1000×Myocardial ATP content was measured using an ATP bioluminescent assay kit (TA100, TOYO Ink, Tokyo, Japan) according to the manufacturer’s instructions.We investigated autophagic flux in vivo using previously described methods.All statistical analyses were performed using Graph Pad PRISM version 6.07 statistical software (GraphPad Software, CA). In addition, cardiac-specific transgenic mice overexpressing a dominant negative (DN) α2 subunit (D157A) of AMPK (DN-AMPKα2, a gift of Rong Tian, University of Washington, Seattle, WA), aged 8 weeks old, were rendered diabetic by five consecutive daily injections of streptozotocin (STZ, 50 mg/kg i.p. Hiromitsu Kanamori, MD, Department of Cardiology, Gifu University Graduate School of Medicine, 1-1 Yanagido, Gifu 501–1194, Japan. ), Oklahoma Center for the Advancement of Science and Technology (M.-H.Z. Eugene Patterson and Xichun Yu, Department of Medicine, the University of Oklahoma Health Sciences Center, for technical support.Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. Thus, stimulation of AMPK may represent a novel approach to treat diabetic cardiomyopathy.This study was supported by funding from the National Institutes of Health grants (HL-079584, HL-080499, HL-074399, HL-089920, and HL-096032 to M.-H.Z. Data are expressed as means±1 SD. Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34)Thiazolidinediones, metformin, and outcomes in older patients with diabetes and heart failure: an observational study.Metformin and thiazolidinedione use in Medicare patients with heart failure.Metformin prevents progression of heart failure in dogs: role of AMP-activated protein kinase.Activation of AMP-activated protein kinase by metformin improves left ventricular function and survival in heart failure.Metformin improves cardiac function in a nondiabetic rat model of post-MI heart failure.Metformin increases peroxisome proliferator-activated receptor γ Co-activator-1α and utrophin a expression in dystrophic skeletal muscle.The variability of autophagy and cell death susceptibility: unanswered questions.Autophagic degeneration and death of cardiomyocytes in heart failure.The role of autophagy in cardiomyocytes in the basal state and in response to hemodynamic stress.Resveratrol reverses remodeling in hearts with large, old myocardial infarctions through enhanced autophagy-activating AMP kinase pathway.Autophagic adaptations in diabetic cardiomyopathy differ between type 1 and type 2 diabetes.Differential requirement for individual sarcoglycans and dystrophin in the assembly and function of the dystrophin-glycoprotein complex.Muscular dystrophies involving the dystrophin-glycoprotein complex: an overview of current mouse models.A method to measure cardiac autophagic flux in vivo.Sarcoglycan complex: implications for metabolic defects in muscular dystrophies.Expression of full-length utrophin prevents muscular dystrophy in mdx mice.LC3, a mammalian homologue of yeast Apg8p, is localized in autophagosome membranes after processing.Homeostatic levels of p62 control cytoplasmic inclusion body formation in autophagy-deficient mice.Histological parameters for the quantitative assessment of muscular dystrophy in the mdx-mouse.Utrophin A is essential in mediating the functional adaptations of mdx mouse muscle following chronic AMPK activation.Animal models for muscular dystrophy show different patterns of sarcolemmal disruption.Disruption of the sarcoglycan-sarcospan complex in vascular smooth muscle: a novel mechanism for cardiomyopathy and muscular dystrophy.Functional significance and morphological characterization of starvation-induced autophagy in the adult heart.Autophagy limits acute myocardial infarction induced by permanent coronary artery occlusion.Metformin effects on the heart and the cardiovascular system: a review of experimental and clinical data.Role of AMP-activated protein kinase in mechanism of metformin action.LKB1 and AMP-activated protein kinase control of mTOR signalling and growth.Improvement of cardiac functions by chronic metformin treatment is associated with enhanced cardiac autophagy in diabetic OVE26 mice.Metformin attenuates cardiac fibrosis by inhibiting the TGFbeta1-Smad3 signalling pathway.Metformin protects against systolic overload-induced heart failure independent of AMP-activated protein kinase α2.

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