| Impaired TCA cycle flux in mitochondria in skeletal muscle from type 2 diabetic subjects: Marker or maker of the diabetic phenotype? | |
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MedLine Citation:
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PMID: 22385297 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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The diabetic phenotype is complex, requiring elucidation of key initiating defects. Recent research has shown that diabetic myotubes express a primary reduced tricarboxylic acid (TCA) cycle flux. A reduced TCA cycle flux has also been shown both in insulin resistant offspring of T2D patients and exercising T2D patients in vivo. This review will discuss the latest advances in the understanding of the molecular mechanisms regulating the TCA cycle with focus on possible underlying mechanism which could explain the impaired TCA flux in insulin resistant human skeletal muscle in type 2 diabetes. A reduced TCA is both a marker and a maker of the diabetic phenotype. |
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Authors:
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Michael Gaster; Jan O Nehlin; Ariane D Minet |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-3-5 |
Journal Detail:
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Title: Archives of physiology and biochemistry Volume: - ISSN: 1744-4160 ISO Abbreviation: - Publication Date: 2012 Mar |
Date Detail:
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Created Date: 2012-3-5 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9510153 Medline TA: Arch Physiol Biochem Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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Laboratory of Molecular Physiology, Department of Pathology , Denmark. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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