rdf:type |
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lifeskim:mentions |
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pubmed:issue |
7
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pubmed:dateCreated |
2011-6-28
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pubmed:abstractText |
Overactivity of the Forkhead transcription factor FoxO1 promotes diabetic hyperglycemia, dyslipidemia, and acute-phase response, whereas suppression of FoxO1 activity by insulin may alleviate diabetes. The reported efficacy of long-chain fatty acyl (LCFA) analogs of the MEDICA series in activating AMP-activated protein kinase (AMPK) and in treating animal models of diabesity may indicate suppression of FoxO1 activity.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
1939-327X
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pubmed:author |
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pubmed:copyrightInfo |
© 2011 by the American Diabetes Association.
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pubmed:issnType |
Electronic
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pubmed:volume |
60
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1872-81
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:21602511-AMP-Activated Protein Kinases,
pubmed-meshheading:21602511-Acute-Phase Reaction,
pubmed-meshheading:21602511-Animals,
pubmed-meshheading:21602511-C-Reactive Protein,
pubmed-meshheading:21602511-CCAAT-Enhancer-Binding Protein-beta,
pubmed-meshheading:21602511-COS Cells,
pubmed-meshheading:21602511-Cercopithecus aethiops,
pubmed-meshheading:21602511-Dicarboxylic Acids,
pubmed-meshheading:21602511-Forkhead Transcription Factors,
pubmed-meshheading:21602511-Guinea Pigs,
pubmed-meshheading:21602511-Hep G2 Cells,
pubmed-meshheading:21602511-Humans,
pubmed-meshheading:21602511-Insulin,
pubmed-meshheading:21602511-Male,
pubmed-meshheading:21602511-Metformin,
pubmed-meshheading:21602511-Mice,
pubmed-meshheading:21602511-Mice, Transgenic,
pubmed-meshheading:21602511-STAT3 Transcription Factor
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pubmed:year |
2011
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pubmed:articleTitle |
Suppression of FoxO1 activity by long-chain fatty acyl analogs.
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pubmed:affiliation |
Department of Human Nutrition and Metabolism, Hebrew University Medical School, Jerusalem, Israel.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
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