Endocrinol Metab.  2017 Jun;32(2):171-179. 10.3803/EnM.2017.32.2.171.

Diabetes-Related Cardiac Dysfunction

• Williams L
• Nye BG
• Wende AR

• KMID: 2384075
• DOI: http://doi.org/10.3803/EnM.2017.32.2.171

Abstract

The proposal that diabetes plays a role in the development of heart failure is supported by the increased risk associated with this disease, even after correcting for all other known risk factors. However, the precise mechanisms contributing to the condition referred to as diabetic cardiomyopathy have remained elusive, as does defining the disease itself. Decades of study have defined numerous potential factors that each contribute to disease susceptibility, progression, and severity. Many recent detailed reviews have been published on mechanisms involving insulin resistance, dysregulation of microRNAs, and increased reactive oxygen species, as well as causes including both modifiable and non-modifiable risk factors. As such, the focus of the current review is to highlight aspects of each of these topics and to provide specific examples of recent advances in each area.

Keyword

Diabetic cardiomyopathies; Energy metabolism; Heart failure; Metabolic diseases; Mitochondria, heart; Stress, physiological

MeSH Terms

Diabetic Cardiomyopathies
Disease Susceptibility
Energy Metabolism
Heart Failure
Insulin Resistance
Metabolic Diseases
MicroRNAs
Mitochondria, Heart
Reactive Oxygen Species
Risk Factors
Stress, Physiological
MicroRNAs
Reactive Oxygen Species

Figure

• 

  Fig. 1 Diabetic cardiomyopathy: causes, consequences, and outcomes. A schematic summary of modifiable and non-modifiable risk factors discussed in the text that contribute to development of diabetic cardiomyopathy. Diabetes is characterized by hyperglycemia and systemic changes, including inflammation and reduced cardiac contractility. These systemic changes are mediated through cellular changes including fibrosis and altered mitochondrial metabolism, including decreased glucose oxidation (GLOX) and increased fatty acid oxidation (FAO), which can in turn mediate exacerbated levels of reactive oxygen species (ROS) and protein O-GlcNAcylation contributing to decreased cellular function and disrupted gene expression. Ultimately, these structural, cellular, and molecular changes contribute to decreased cardiac function and the subsequent development of diabetic cardiomyopathy. Modified from Servier Medical Art (http://www.servier.com). AGE, advanced glycation end product; O-GlcNAc, O-linked β-N-acetylglucosamine; Glc, glucose; FA, fatty acid.

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