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Insulin resistance and increased lipolysis in bone marrow derived adipocytes stimulated with agonists of Toll-like receptors

Franchini, M. and Monnais, E. and Seboek, D. and Radimerski, T. and Zini, E. and Kaufmann, K. and Lutz, T. and Reusch, C. and Ackermann, M. and Muller, B. and Linscheid, P.. (2010) Insulin resistance and increased lipolysis in bone marrow derived adipocytes stimulated with agonists of Toll-like receptors. Hormone and Metabolic Research, 42 (10). pp. 703-709.

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Official URL: http://edoc.unibas.ch/56779/

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Abstract

Our objectives were to identify Toll-like receptors (TLRs) in human bone marrow derived adipocytes, to test specific TLR agonists for their ability to induce a proinflammatory response, and to investigate possible metabolic effects after TLR activation, in particular, those associated with insulin resistance and lipolysis. Mesenchymal stem cells were isolated from human bone marrow and differentiated into adipocytes. Total RNA before or after stimulation with agonists specific for TLR was extracted for analysis of expression of TLRs proinflammatory signals and molecules involved in glucose metabolism (IRS-1 and GLUT4). Furthermore, cytokine protein expression was measured from cell lysates. Finally, insulin induced glucose uptake and lipolysis were measured. Human bone marrow-derived adipocytes express TLR1-10. They react to stimulation with specific ligands with expression of inflammatory markers (IL-1beta, IL-6, TNFalpha, IL-8, MCP-1) at the RNA and protein levels. IRS-1 and GLUT4 expression was downregulated after stimulation with the TLR4 and TLR3 specific ligands LPS and poly (I:C), respectively. Insulin-induced glucose uptake was decreased and lipolysis increased. We conclude that adipocytes express TLR 1-10 and react to agonists specific for TLR 1-6. As a consequence proinflammatory cytokine are induced, in particular, IL-6, IL-8, and MCP-1. Since stimulation is followed by decreased insulin-induced glucose uptake and increased lipolysis we conclude that TLRs may be important linking molecules in the generation of insulin resistance in fat tissue.
Faculties and Departments:03 Faculty of Medicine > Bereich Medizinische Fächer (Klinik) > Allgemeine innere Medizin AG > Argovia Professur für Medizin (Müller)
03 Faculty of Medicine > Departement Klinische Forschung > Bereich Medizinische Fächer (Klinik) > Allgemeine innere Medizin AG > Argovia Professur für Medizin (Müller)
UniBasel Contributors:Müller, Beat
Item Type:Article, refereed
Article Subtype:Research Article
Publisher:Georg Thieme Verlag
ISSN:0018-5043
e-ISSN:1439-4286
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:29 Nov 2017 11:05
Deposited On:29 Nov 2017 11:05

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