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Review
. 2013 Nov 25;2(6):e000433.
doi: 10.1161/JAHA.113.000433.

Taking diabetes to heart--deregulation of myocardial lipid metabolism in diabetic cardiomyopathy

Marina Bayeva  1 , Konrad Teodor Sawicki, Hossein Ardehali
Affiliations
Review

Taking diabetes to heart--deregulation of myocardial lipid metabolism in diabetic cardiomyopathy

Marina Bayeva et al. J Am Heart Assoc. .
No abstract available

Keywords: diabetes mellitus; diabetic cardiomyopathy; lipid toxicity; lipids and lipoprotein metabolism.

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Figures

Figure 1.
Figure 1.
Overview of myocardial fatty acid (FA) metabolism. FAs are imported into the cell by various FA transporters, including CD36, FA transport protein (FATP), and plasma membrane FA‐binding protein (FABPpm). Imported FAs may be stored as triglyceride (TAG) or converted to fatty acyl CoA by FA CoA synthase (FACS). The acyl group of fatty acid CoA can be transferred to carnitine via carnitine palmitoyltransferase (CPT) 1. The acylcarnitine is then shuttled into the mitochondria by carnitine translocase (CT), where it can undergo β‐oxidation, producing acetyl CoA, which can be used in the tricarboxylic acid (TCA) cycle to produce adenosine triphosphate (ATP).
Figure 2.
Figure 2.
Pathophysiology of type 1 (T1DM) and type 2 (T2DM) diabetes mellitus on energy metabolism in the heart. Both T1DM and T2DM lead to insulin receptor substrate 1 (IRS1) inhibition, peroxisome proliferator‐activated receptor α (PPARα) activation, and suppression of glycolysis, resulting in metabolic rigidity, reduced adenosine triphosphate (ATP) generation efficiency, and generation of toxic fatty acid (FA) intermediates. PDK4 indicates pyruvate dehydrogenase kinase 4.
See this image and copyright information in PMC

References

    1. CDC National Diabetes Fact Sheet: National Estimates and General Information on Diabetes and Prediabetes in the United States, 2011. 2011Atlanta, GA: U.S. Department of Health and Human Services CfDCaP, ed
    1. Garcia MJ, McNamara PM, Gordon T, Kannel WB. Morbidity and mortality in diabetics in the Framingham population. Sixteen year follow‐up study. Diabetes. 1974; 23:105-111 - PubMed
    1. Haffner SM, Lehto S, Ronnemaa T, Pyorala K, Laakso M. Mortality from coronary heart disease in subjects with type 2 diabetes and in nondiabetic subjects with and without prior myocardial infarction. N Engl J Med. 1998; 339:229-234 - PubMed
    1. Moller DE, Kaufman KD. Metabolic syndrome: a clinical and molecular perspective. Annu Rev Med. 2005; 56:45-62 - PubMed
    1. Cornier MA, Dabelea D, Hernandez TL, Lindstrom RC, Steig AJ, Stob NR, Van Pelt RE, Wang H, Eckel RH. The metabolic syndrome. Endocr Rev. 2008; 29:777-822 - PMC - PubMed

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