Document Detail


Establishment of new highly insulin-sensitive cell lines and screening of compounds to facilitate glucose consumption.
MedLine Citation:
PMID:  19008648     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Kenji Hayata; Katsuichi Sakano; Shigeyuki Nishinaka
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Publication Detail:
Type:  Journal Article     Date:  2008-11-13
Journal Detail:
Title:  Journal of pharmacological sciences     Volume:  108     ISSN:  1347-8613     ISO Abbreviation:  J. Pharmacol. Sci.     Publication Date:  2008 Nov 
Date Detail:
Created Date:  2008-11-21     Completed Date:  2009-01-07     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  101167001     Medline TA:  J Pharmacol Sci     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  348-54     Citation Subset:  IM    
Affiliation:
R&D Division, Exploratory Research Laboratories II, Daiichi-Sankyo Co., Ltd., Tokyo, Japan. hayata.kenji.v6@daiichisankyo.co.jp
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MeSH Terms
Descriptor/Qualifier:
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:
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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