Titlebook: Diabetic Cardiomyopathy; Biochemical and Mole Belma Turan,Naranjan S. Dhalla Book 2014 Springer Science+Business Media New York 2014 Cardio

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Induction of Metabolic Syndrome by Excess Fructose Consumption consumption from overeating. Fructose is now a major component of the Western diet, with increased consumption associated with obesity, metabolic syndrome, and cardiovascular disorders in observational and short-term intervention studies, mainly in animal models. Rodent studies have identified poss

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Substrate Metabolism in the Diabetic Hearted metabolic milieu during diabetes. Constant requirement for energy in the form of ATP is fulfilled mainly by utilizing carbohydrates (glucose and lactate) and fatty acids in the heart. Only minor differences exist between species, and the healthy adult heart relies on the oxidation of fatty acids

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Effects of Diabetes-Induced Hyperglycemia in the Heart: Biochemical and Structural Alterationsllular level and moreover it is an independent risk factor to worsen cardiac performance and cell survival. The heart is a major target organ for damage with hyperglycemia. Alterations as a result of HG can lead to the development of a diabetic cardiomyopathy, resulting in changes to cardiac structu

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Hyperglycemia, Oxidative Stress, and Vascular Complications: Role of Epigenetic Mechanisms. Although the metabolic disturbances such as oxidative stress, inflammation, and hyperlipidemia have been well described as main players in the process of vascular dysfunction, epigenetic modifications of gene expression also occur under the hyperglycemic state and modulate cardiovascular homeostas

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Aldose Reductase and Diabetic Cardiovascular Disease aldose reductase (AR) as a key player in mediating diabetic cardiovascular complications. Findings by us and others demonstrate that increased flux via AR in diabetics perpetuates increased injury after myocardial infarction, accelerates atherosclerotic lesion formation, and promotes restenosis via

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MicroRNomics of Diabetic Cardiomyopathyere they target 3′-UTR and degrade mRNA or repress translation, or by RNA activation (RNAa), where they target promoter elements at 5′-UTR and induce gene transcription. They have emerged as a therapeutic target for diabetes and cardiovascular diseases because each miRNA has several targets that all