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Beijing Institute of Hepatology, Beijing, China
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Beijing Lab for Cardiovascular Precision Medicine, Beijing, China
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Introduction Diabetic cardiomyopathy is known to be a special form of heart disease, first proposed by Rubler et al. (1972) , and its typical definition includes abnormal structural and functional abnormalities in the myocardium of diabetic
Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada
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Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada
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Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada
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Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada
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Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada
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Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada
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Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada
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Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada
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Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada
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Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada
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Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada
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Gandhi M Eaton F , et al. 2021 The GLP-1 receptor agonist liraglutide increases myocardial glucose oxidation rates via indirect mechanisms and mitigates experimental diabetic cardiomyopathy . Canadian Journal of Cardiology 37 140 – 150 . ( https
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Introduction Diabetic cardiomyopathy (DCM) induced by diabetes is increasingly recognized as the most important cause of elevated morbidity and mortality among diabetic patients ( Chavali et al . 2013 ). DCM is characterized by abnormalities
Department of Endocrinology, The Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China
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Introduction Diabetic cardiomyopathy (DCM) is a major cardiovascular complication of diabetes mellitus, in which heart structural impairment and functional deficits lead to heart failure ( Zhou et al. 2018 ). DCM is characterized by
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Introduction In humans and animal models of diabetes, a heart muscle-specific disease in the absence of any vascular pathology has been described, and termed diabetic cardiomyopathy ( Picano 2003 , Avogaro et al . 2004 ). The pathogenesis of
Cardiac Electrophysiology Research and Training Center, Cardiac Electrophysiology Unit, Center of Excellence in Cardiac Electrophysiology Research, Department of Oral Biology and Diagnostic Sciences, Faculty of Medicine
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Cardiac Electrophysiology Research and Training Center, Cardiac Electrophysiology Unit, Center of Excellence in Cardiac Electrophysiology Research, Department of Oral Biology and Diagnostic Sciences, Faculty of Medicine
Cardiac Electrophysiology Research and Training Center, Cardiac Electrophysiology Unit, Center of Excellence in Cardiac Electrophysiology Research, Department of Oral Biology and Diagnostic Sciences, Faculty of Medicine
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Cardiac Electrophysiology Research and Training Center, Cardiac Electrophysiology Unit, Center of Excellence in Cardiac Electrophysiology Research, Department of Oral Biology and Diagnostic Sciences, Faculty of Medicine
Cardiac Electrophysiology Research and Training Center, Cardiac Electrophysiology Unit, Center of Excellence in Cardiac Electrophysiology Research, Department of Oral Biology and Diagnostic Sciences, Faculty of Medicine
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development of diabetic cardiomyopathy (DCM) ( Yan et al . 2015 ). In contrast, FGF21 administration also prevents lipotoxicity and diabetes induced cardiac apoptosis in DCM ( Zhang et al . 2015a ). Interestingly, Liu and colleague demonstrated that the
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structural damage and functional loss ( Battiprolu et al . 2010 ). All of the factors often interact with each other therefore making T2D a complex disease to treat. In the early 1970s, the concept of diabetic cardiomyopathy was recognized on the basis of
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Diabetic cardiomyopathy is characterized by cardiac dysfunction and altered level/function of insulin-like growth factor I (IGF-I). Both endogenous and exogenous IGF-I have been shown to effectively alleviate diabetes-induced cardiac dysfunction and oxidative stress. This study was designed to examine the effect of cardiac overexpression of IGF-I on streptozotocin (STZ)-induced cardiac contractile dysfunction in mouse myocytes. Both IGF-I heterozygous transgenic mice and their wild-type FVB littermates were made diabetic with a single injection of STZ (200 mg/kg, i.p.) and maintained for 2 weeks. The following mechanical indices were evaluated in ventricular myocytes: peak shortening (PS), time-to-PS (TPS), time-to-90% relengthening (TR90) and maximal velocity of shortening/relengthening (+/- dL/dt). Intracellular Ca2+ was evaluated as resting and peak intracellular Ca2+ levels, Ca2+-induced Ca2+ release and intracellular Ca2+ decay rate (tau). STZ led to hyperglycemia in FVB and IGF-I mice. STZ treatment prolonged TPS and TR90, reduced Ca2+-induced Ca2+ release, increased resting intracellular Ca2+ levels and slowed tau associated with normal PS and +/- dL/dt. All of which, except the elevated resting intracellular Ca2+, were prevented by the IGF-I transgene. In addition, myocytes from STZ-treated FVB mice displayed an attenuated contractile response to the beta-adrenergic agonist isoproterenol, which was restored by the IGF-I transgene. Contractile response to the alpha-adrenergic agonist phenylephrine and angiotensin II was not affected by either STZ treatment or IGF-I. These results validate the beneficial role of IGF-I in diabetic cardiomyopathy, possibly due to an improved beta-adrenergic response.
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Introduction Glucose toxicity contributes to development of diabetic cardiomyopathy characterized by systolic and diastolic dysfunctions independent of coronary macro- and micro-vascular diseases ( Galderisi et al. 1991 , Ren et
Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
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Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
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Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
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with a cardiac-specific overexpression of PPARα exhibit decreased myocardial glucose oxidation rates and a diabetic cardiomyopathy phenotype ( Finck et al. 2002 ). In addition, studies have also demonstrated that forkhead box O1 (FoxO1) is another
