Korean Diabetes J.  2008 Dec;32(6):467-473. 10.4093/kdj.2008.32.6.467.

Mitochondrial Dysfunction in Diabetic Cardiomyopathy

• Ahn JH
• Kim JT

• KMID: 2222453
• DOI: http://doi.org/10.4093/kdj.2008.32.6.467

Abstract

Metabolic syndrome and diabetes are associated with increased risk of cardiac dysfunction independently of underlying coronary artery disease. The underlying pathogenesis is partially understood but accumulating evidence suggests that alterations of cardiac energy metabolism might contribute to the development of contractile dysfunction. Recent findings suggest that myocardial mitochondrial dysfunction may play an important role in the pathogenesis of cardiac contractile dysfunction in type 2 diabetes. This review is focused on evaluating mechanisms for the mitochondrial abnormalities that may be involved in the development and progression of cardiac dysfunction in diabetes.

Keyword

Cardiac Dysfunction; Diabetes; Energy Metabolism; Mitochondria

MeSH Terms

Coronary Artery Disease
Diabetic Cardiomyopathies
Energy Metabolism
Mitochondria

Figure

• 

  Fig. 1 The proposed mechanism of decreased cardiac efficiency in diabetic heart. Increased serum fatty acid levels and cardiac insulin resistance may lead to increased fatty acid oxidation (FAO) and decreased glucose oxidation (GO). The resulting increase in reducing equivalent delivery to the respiratory chain may increase mitochondrial generation of reactive oxygen species (ROS), which may induce mitochondrial uncoupling by activating uncoupling proteins (UCP) and adenine nucleotide translocator (ANT). This may result in increased mitochondrial oxygen consumption, thereby increasing FAO even further. Increased oxygen consumption in the absence of increased cardiac work caused by a relative energy deficit reduces cardiac efficiency. On the other hand, ROS may also induce oxidative stress to mitochondrial proteins involved in oxidative phosphorylation, thereby reducing ATP synthesis (adapted from reference 44).

• 

  Fig. 2 Increased cardiac mitochondrial proliferation in db/db mice. A. Representative electron micrographs from wild-type (a) and db/db (b) hearts. Magnification ×2000. B. A quantitative analysis of mitochondrial number in each group (wild type or db/db). *P < 0.05 vs. wild type (adapted from reference 37).

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