| Enhancement of TNF-α expression and inhibition of glucose uptake by nicotine in the presence of a free fatty acid in C2C12 skeletal myocytes. | |
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MedLine Citation:
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PMID: 21080305 Owner: NLM Status: In-Process |
Abstract/OtherAbstract:
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Smoking is a risk factor for insulin resistance and metabolic syndrome. However, mechanisms responsible for smoking-induced insulin resistance are unclear. We examined the combined effect of nicotine, a toxic substance in tobacco smoke, and palmitate in the serum physiological concentration range on tumor necrosis factor-α (TNF-α) expression and impairment of glucose uptake in C2C12 myotubes, since smokers do not have increased serum free fatty acid (FFA) concentrations with insulin resistance compared to nonsmokers. C2C12 myotubes were incubated for 24 h with nicotine (1 μmol/l) in the presence or absence of palmitate (200 μmol/l). RT-PCR and Western blotting showed increased TNF-α expression in C2C12 myotubes treated with nicotine in the presence of palmitate. Furthermore, stimulation with nicotine in the presence of palmitate enhanced the production of reactive oxygen species (ROS) and activated the protein kinase C-nuclear factor-κB (PKC-NF-κB) pathway, as detected by dihydroethidium staining and Western blotting, respectively. Consequently, the translocation of GLUT4 to the plasma membrane as well as insulin-stimulated Akt phosphorylation was impaired, and glucose uptake to the myocytes was blocked. In addition, the production of ROS was suppressed by 4-hydroxy-TEMPO, and inhibition of GLUT4 translocation to the plasma membrane was canceled. These results suggest that in C2C12 myotubes, nicotine in the presence of palmitate enhanced the production of ROS and the expression of TNF-α through the PKC-NF-κB pathway; suppressed GLUT4 translocation to the plasma membrane; and impaired glucose uptake to cells. This pathway represents a possible mechanism by which smoking induces insulin resistance in the body. |
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Authors:
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J Tatebe; T Morita |
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Publication Detail:
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Type: Journal Article Date: 2010-11-15 |
Journal Detail:
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Title: Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme Volume: 43 ISSN: 1439-4286 ISO Abbreviation: Horm. Metab. Res. Publication Date: 2011 Jan |
Date Detail:
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Created Date: 2011-01-05 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0177722 Medline TA: Horm Metab Res Country: Germany |
Other Details:
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Languages: eng Pagination: 11-6 Citation Subset: IM |
Copyright Information:
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© Georg Thieme Verlag KG Stuttgart · New York. |
Affiliation:
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Department of Laboratory Medicine, Toho University, Tokyo, Japan. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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