rdf:type |
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lifeskim:mentions |
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pubmed:dateCreated |
2006-7-26
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pubmed:abstractText |
Cardiovascular disease is the primary cause of death in individuals with obesity and diabetes. However, the underlying mechanisms for cardiac dysfunction are partially understood. Studies have suggested that altered cardiac metabolism may play a role. The diabetic heart is characterized by increased fatty acid oxidation, increased myocardial oxygen consumption, and reduced cardiac efficiency. Here, we review possible mechanisms for reduced cardiac efficiency in obesity and diabetes by focusing on the potential role of mitochondrial uncoupling.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1548-9213
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:volume |
21
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
250-8
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pubmed:dateRevised |
2010-1-14
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pubmed:meshHeading |
pubmed-meshheading:16868314-Animals,
pubmed-meshheading:16868314-Carrier Proteins,
pubmed-meshheading:16868314-Diabetes Mellitus, Type 2,
pubmed-meshheading:16868314-Diabetic Angiopathies,
pubmed-meshheading:16868314-Fatty Acids,
pubmed-meshheading:16868314-Heart,
pubmed-meshheading:16868314-Humans,
pubmed-meshheading:16868314-Ion Channels,
pubmed-meshheading:16868314-Membrane Proteins,
pubmed-meshheading:16868314-Mice,
pubmed-meshheading:16868314-Mitochondria, Heart,
pubmed-meshheading:16868314-Mitochondrial ADP, ATP Translocases,
pubmed-meshheading:16868314-Mitochondrial Proteins,
pubmed-meshheading:16868314-Myocardium,
pubmed-meshheading:16868314-Obesity,
pubmed-meshheading:16868314-Oxygen Consumption
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pubmed:year |
2006
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pubmed:articleTitle |
Mitochondrial uncoupling: a key contributor to reduced cardiac efficiency in diabetes.
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pubmed:affiliation |
Division of Endocrinology, Metabolism, and Diabetes, and Program in Human Molecular Biology and Genetics, University of Utah School of Medicine, Salt Lake City, Utah, USA.
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pubmed:publicationType |
Journal Article,
Review,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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