| Establishment of new highly insulin-sensitive cell lines and screening of compounds to facilitate glucose consumption. | |
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MedLine Citation:
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PMID: 19008648 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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To obtain compounds that promote glucose uptake in muscle cells, the novel cell lines A31-IS derived from Balb/c 3T3 A31 and C2C12-IS from mouse myoblast C2C12 were established. In both cell lines, glucose consumption was induced by insulin and suppressed by the addition of Akt-activating kinase inhibitor. The A31-IS cells highly express the insulin receptor beta chains, Glut4, and uncoupling protein-3, as compared to the parent Balb/c 3T3 A31 cells, and C2C12-IS cells highly express the insulin receptor beta chain as compared to its parent cell line. Using A31-IS cells, we screened our library compounds and obtained three compounds, DF-4394, DF-4451, and DG-5451. These compounds dose-dependently promoted glucose consumption in A31-IS cells and facilitated [3H]-2-deoxyglucose uptake in differentiated C2C12-IS cells. The compounds that we obtained from the library screening will be good candidates for improving insulin resistance in muscle cells. |
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Authors:
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Kenji Hayata; Katsuichi Sakano; Shigeyuki Nishinaka |
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Publication Detail:
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Type: Journal Article Date: 2008-11-13 |
Journal Detail:
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Title: Journal of pharmacological sciences Volume: 108 ISSN: 1347-8613 ISO Abbreviation: J. Pharmacol. Sci. Publication Date: 2008 Nov |
Date Detail:
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Created Date: 2008-11-21 Completed Date: 2009-01-07 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 101167001 Medline TA: J Pharmacol Sci Country: Japan |
Other Details:
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Languages: eng Pagination: 348-54 Citation Subset: IM |
Affiliation:
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R&D Division, Exploratory Research Laboratories II, Daiichi-Sankyo Co., Ltd., Tokyo, Japan. hayata.kenji.v6@daiichisankyo.co.jp |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals BALB 3T3 Cells Cell Separation Dose-Response Relationship, Drug Glucose / metabolism* Glucose Transporter Type 4 / metabolism Hypoglycemic Agents / pharmacology* Insulin / metabolism* Insulin Resistance* Ion Channels / metabolism Mice Mitochondrial Proteins / metabolism Muscle Cells / drug effects*, enzymology, metabolism Protein Kinase Inhibitors / pharmacology Proto-Oncogene Proteins c-akt / metabolism Receptor, Insulin / metabolism Small Molecule Libraries |
| Chemical | |
Reg. No./Substance:
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0/Glucose Transporter Type 4; 0/Hypoglycemic Agents; 0/Ion Channels; 0/Mitochondrial Proteins; 0/Protein Kinase Inhibitors; 0/Slc2a4 protein, mouse; 0/Small Molecule Libraries; 0/mitochondrial uncoupling protein 3; 11061-68-0/Insulin; 50-99-7/Glucose; EC 2.7.10.1/Receptor, Insulin; EC 2.7.11.1/Proto-Oncogene Proteins c-akt |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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