| Adiponectin gene expression and secretion is inhibited by interleukin-6 in 3T3-L1 adipocytes. | |
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MedLine Citation:
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PMID: 12589818 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Recently, it has been shown that adiponectin is an important insulin-sensitizing fat-derived protein which is downregulated in insulin resistance and obesity, and replenishment of which improves insulin sensitivity. In contrast, interleukin (IL)-6 appears as an adipocytokine serum concentrations of which are elevated in these states. However, it has not been determined whether IL-6 might impact on expression and secretion of adiponectin. To clarify this, 3T3-L1 adipocytes were treated with different concentrations of IL-6 for various periods of time. Adiponectin mRNA was measured by quantitative real-time reverse transcription-polymerase chain reaction and secretion was determined by radioimmunoassays. Interestingly, treatment of 3T3-L1 cells with 30 ng/ml IL-6 significantly decreased adiponectin secretion to 75% of control levels. Adiponectin secretion was also inhibited between 25% and 45% by chronic treatment with forskolin (50 microM), tumor necrosis factor alpha (100 ng/ml), and dexamethasone (100 nM). Furthermore, adiponectin mRNA expression was downregulated by up to 50% in a time- and dose-dependent manner, with significant inhibition detectable at concentrations as low as 3 ng/ml IL-6 and as early as 8h after effector addition. The inhibitory effect of IL-6 was partially reversed by pretreatment of 3T3-L1 cells with pharmacological inhibitors of a p44/42 mitogen-activated protein (MAP) kinase. Moreover, the negative effect of IL-6 on adiponectin mRNA expression could be reversed by withdrawal of the hormone for 24h. Taken together, our results suggest that adiponectin gene expression is reversibly downregulated by IL-6 and support the concept of adiponectin being an important selectively controlled modulator of insulin sensitivity. |
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Authors:
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Mathias Fasshauer; Susan Kralisch; Margit Klier; Ulrike Lossner; Matthias Bluher; Johannes Klein; Ralf Paschke |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Biochemical and biophysical research communications Volume: 301 ISSN: 0006-291X ISO Abbreviation: Biochem. Biophys. Res. Commun. Publication Date: 2003 Feb |
Date Detail:
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Created Date: 2003-02-18 Completed Date: 2003-04-09 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 0372516 Medline TA: Biochem Biophys Res Commun Country: United States |
Other Details:
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Languages: eng Pagination: 1045-50 Citation Subset: IM |
Affiliation:
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Department of Internal Medicine III, University of Leipzig, Ph.-Rosenthal-Str. 27, 04103, Leipzig, Germany. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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3T3 Cells Adipocytes / drug effects*, metabolism* Adiponectin Animals Dexamethasone / pharmacology Down-Regulation / drug effects Forskolin / pharmacology Gene Expression / drug effects Insulin Resistance / physiology Intercellular Signaling Peptides and Proteins* Interleukin-6 / pharmacology* Mice Mitogen-Activated Protein Kinase 1 / metabolism Mitogen-Activated Protein Kinase 3 Mitogen-Activated Protein Kinases / metabolism Protein Biosynthesis* Proteins / genetics* RNA, Messenger / genetics, metabolism Tumor Necrosis Factor-alpha / pharmacology |
| Chemical | |
Reg. No./Substance:
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0/Adiponectin; 0/Intercellular Signaling Peptides and Proteins; 0/Interleukin-6; 0/Proteins; 0/RNA, Messenger; 0/Tumor Necrosis Factor-alpha; 50-02-2/Dexamethasone; 66428-89-5/Forskolin; EC 2.7.11.24/Mitogen-Activated Protein Kinase 1; EC 2.7.11.24/Mitogen-Activated Protein Kinase 3; EC 2.7.11.24/Mitogen-Activated Protein Kinases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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