Subject    :    [2017 Feb;41(1)] My Sweetheart Is Broken: Role of Glucose in Diabetic Cardiomyopathy
Writer KDA
Date 2017-03-23 10:30:49 Hit 4,025
Diabetes Metab J. 2017 Feb;41(1):1-9. English. Published online Nov 15, 2016.  https://doi.org/10.4093/dmj.2017.41.1.1 
Copyright © 2017 Korean Diabetes Association
   
My Sweetheart Is Broken: Role of Glucose in Diabetic Cardiomyopathy
Manoja K. Brahma,1 Mark E. Pepin,1,2 and Adam R. Wende1
1Division of Molecular and Cellular Pathology, Department of Pathology, The University of Alabama at Birmingham, Birmingham, AL, USA.
2Department of Biomedical Engineering, The University of Alabama at Birmingham, Birmingham, AL, USA.
Corresponding author: Adam R. Wende. Division of Molecular and Cellular Pathology, Department of Pathology, The University of Alabama at Birmingham, BMR2, Office 506, 901 19th Street South, Birmingham, AL 35294-2180 USA. Email: adamwende@uabmc.edu 
 
Received September 23, 2016; Accepted October 11, 2016.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

 
Abstract

Despite overall reductions in heart disease prevalence, the risk of developing heart failure has remained 2-fold greater among people with diabetes. Growing evidence has supported that fluctuations in glucose level and uptake contribute to cardiovascular disease (CVD) by modifying proteins, DNA, and gene expression. In the case of glucose, clinical studies have shown that increased dietary sugars for healthy individuals or poor glycemic control in diabetic patients further increased CVD risk. Furthermore, even after decades of maintaining tight glycemic control, susceptibility to disease progression can persist following a period of poor glycemic control through a process termed "glycemic memory." In response to chronically elevated glucose levels, a number of studies have identified molecular targets of the glucose-mediated protein posttranslational modification by the addition of an O-linked N-acetylglucosamine to impair contractility, calcium sensitivity, and mitochondrial protein function. Additionally, elevated glucose contributes to dysfunction in coupling glycolysis to glucose oxidation, pentose phosphate pathway, and polyol pathway. Therefore, in the "sweetened" environment associated with hyperglycemia, there are a number of pathways contributing to increased susceptibly to "breaking" the heart of diabetics. In this review we will discuss the unique contribution of glucose to heart disease and recent advances in defining mechanisms of action.

   
Keywords:
Cardiomyopathies; Diabetes; Glucose; Metabolism
 

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