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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
13
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pubmed:dateCreated |
2010-4-1
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pubmed:abstractText |
c-Jun N-terminal kinase (JNK) 1-dependent signaling plays a crucial role in the development of obesity-associated insulin resistance. Here we demonstrate that JNK activation not only occurs in peripheral tissues, but also in the hypothalamus and pituitary of obese mice. To resolve the importance of JNK1 signaling in the hypothalamic/pituitary circuitry, we have generated mice with a conditional inactivation of JNK1 in nestin-expressing cells (JNK1(DeltaNES) mice). JNK1(DeltaNES) mice exhibit improved insulin sensitivity both in the CNS and in peripheral tissues, improved glucose metabolism, as well as protection from hepatic steatosis and adipose tissue dysfunction upon high-fat feeding. Moreover, JNK1(DeltaNES) mice also show reduced somatic growth in the presence of reduced circulating growth hormone (GH) and insulin-like growth factor 1 (IGF1) concentrations, as well as increased thyroid axis activity. Collectively, these experiments reveal an unexpected, critical role for hypothalamic/pituitary JNK1 signaling in the coordination of metabolic/endocrine homeostasis.
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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 |
Mar
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pubmed:issn |
1091-6490
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pubmed:author |
pubmed-author:BelgardtBengt FBF,
pubmed-author:BrönnekeHella SHS,
pubmed-author:BrüningJens CJC,
pubmed-author:BrodesserSusanneS,
pubmed-author:ErnstMarianne BMB,
pubmed-author:HampelBrigitteB,
pubmed-author:MauerJanJ,
pubmed-author:PalMartinM,
pubmed-author:SchaussAstrid CAC,
pubmed-author:SpohnGabrieleG,
pubmed-author:WunderlichF ThomasFT
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pubmed:issnType |
Electronic
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pubmed:day |
30
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pubmed:volume |
107
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6028-33
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:20231445-Adiposity,
pubmed-meshheading:20231445-Animals,
pubmed-meshheading:20231445-Body Weight,
pubmed-meshheading:20231445-Dietary Fats,
pubmed-meshheading:20231445-Glucose,
pubmed-meshheading:20231445-Growth Hormone,
pubmed-meshheading:20231445-Hypothalamo-Hypophyseal System,
pubmed-meshheading:20231445-Hypothalamus,
pubmed-meshheading:20231445-Insulin,
pubmed-meshheading:20231445-Insulin Resistance,
pubmed-meshheading:20231445-Intermediate Filament Proteins,
pubmed-meshheading:20231445-Mice,
pubmed-meshheading:20231445-Mice, Obese,
pubmed-meshheading:20231445-Mice, Transgenic,
pubmed-meshheading:20231445-Mitogen-Activated Protein Kinase 8,
pubmed-meshheading:20231445-Nerve Tissue Proteins,
pubmed-meshheading:20231445-Pituitary Gland,
pubmed-meshheading:20231445-Signal Transduction,
pubmed-meshheading:20231445-Thyroid Gland
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pubmed:year |
2010
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pubmed:articleTitle |
Hypothalamic and pituitary c-Jun N-terminal kinase 1 signaling coordinately regulates glucose metabolism.
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pubmed:affiliation |
Department of Mouse Genetics and Metabolism, Institute for Genetics, Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases and Center of Molecular Medicine Cologne, University of Cologne, D-50674 Cologne, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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