Document Detail

The relationship between GPR40 and lipotoxicity of the pancreatic β-cells as well as the effect of pioglitazone.
MedLine Citation:
PMID:  21036144     Owner:  NLM     Status:  MEDLINE    
Free fatty acids (FFAs) acutely stimulate insulin secretion from pancreatic β-cells, whereas impair β-cell function following long term exposure. GPR40, a FFAs receptor, has been demonstrated to be activated by both medium and long chain FFAs and played an important role in insulin release. This study was performed to determine the contribution of GPR40 to short- and/or long-term effects of FFAs on glucose-stimulated insulin secretion (GSIS) and the expression of PDX-1 and GLUT2 in pancreatic β-cells, as well as the intervenient effects of pioglitazone on lipotoxicity of β-cells. βTC6 cell line stably expressing GPR40shRNA were established and the intervention of FFAs and pioglitazone on GSIS and expression of PDX-1 and GLUT2 in βTC6 cells was investigated. Results showed that 1-h exposure to FFAs significantly enhanced GSIS and increased expression of PDX-1 and GLUT2 in pSilencer-control transfected cells, but not in cells transfected with GPR40shRNA. While 48-h exposure to FFAs significantly impaired GSIS in pSilencer-control transfected cells as well as cells transfected with GPR40shRNA. Furthermore, pioglitazone enhanced insulin secretion in pSilencer-control transfected cells exposed to FFAs for 48h, but not in cells transfected with GPR40shRNA. These results indicate that GPR40 mediates the short-term effects of FFAs on GSIS, but does not mediate the chronic lipotoxicity on β-cells. The reverse role of pioglitazone on lipotoxicity of β-cells may be related to GPR40.
Peiwen Wu; Liyong Yang; Ximei Shen
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Publication Detail:
Type:  Journal Article     Date:  2010-10-29
Journal Detail:
Title:  Biochemical and biophysical research communications     Volume:  403     ISSN:  1090-2104     ISO Abbreviation:  Biochem. Biophys. Res. Commun.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-12-06     Completed Date:  2011-01-13     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0372516     Medline TA:  Biochem Biophys Res Commun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  36-9     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier Inc. All rights reserved.
Department of Endocrinology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian 350005, China.
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MeSH Terms
Cell Line, Tumor
Fatty Acids, Nonesterified / metabolism,  toxicity*
Gene Knockdown Techniques
Glucose / metabolism,  pharmacology
Hypoglycemic Agents / pharmacology
Insulin / secretion
Insulin-Secreting Cells / drug effects*,  metabolism*,  secretion
Plasmids / genetics
Receptors, G-Protein-Coupled / genetics,  metabolism*
Thiazolidinediones / pharmacology
Reg. No./Substance:
0/Fatty Acids, Nonesterified; 0/Gpr40 protein, mouse; 0/Hypoglycemic Agents; 0/Receptors, G-Protein-Coupled; 0/Thiazolidinediones; 11061-68-0/Insulin; 111025-46-8/pioglitazone; 50-99-7/Glucose

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