Document Detail


Glucagon-like peptide-1 agonists protect pancreatic beta-cells from lipotoxic endoplasmic reticulum stress through upregulation of BiP and JunB.
MedLine Citation:
PMID:  19720788     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: Chronic exposure of pancreatic beta-cells to saturated free fatty acids (FFAs) causes endoplasmic reticulum (ER) stress and apoptosis and may contribute to beta-cell loss in type 2 diabetes. Here, we evaluated the molecular mechanisms involved in the protection of beta-cells from lipotoxic ER stress by glucagon-like peptide (GLP)-1 agonists utilized in the treatment of type 2 diabetes.
RESEARCH DESIGN AND METHODS: INS-1E or fluorescence-activated cell sorter-purified primary rat beta-cells were exposed to oleate or palmitate with or without the GLP-1 agonist exendin-4 or forskolin. Cyclopiazonic acid was used as a synthetic ER stressor, while the activating transcription factor 4-C/EBP homologous protein branch was selectively activated with salubrinal. The ER stress signaling pathways modulated by GLP-1 agonists were studied by real-time PCR and Western blot. Knockdown by RNA interference was used to identify mediators of the antiapoptotic GLP-1 effects in the ER stress response and downstream mitochondrial cell death mechanisms.
RESULTS: Exendin-4 and forskolin protected beta-cells against FFAs via the induction of the ER chaperone BiP and the antiapoptotic protein JunB that mediate beta-cell survival under lipotoxic conditions. On the other hand, exendin-4 and forskolin protected against synthetic ER stressors by inactivating caspase 12 and upregulating Bcl-2 and X-chromosome-linked inhibitor of apoptosis protein that inhibit mitochondrial apoptosis.
CONCLUSIONS: These observations suggest that GLP-1 agonists increase in a context-dependent way the beta-cell defense mechanisms against different pathways involved in ER stress-induced apoptosis. The identification of the pathways modulated by GLP-1 agonists allows for targeted approaches to alleviate beta-cell ER stress in diabetes.
Authors:
Daniel A Cunha; Laurence Ladrière; Fernanda Ortis; Mariana Igoillo-Esteve; Esteban N Gurzov; Roberto Lupi; Piero Marchetti; Décio L Eizirik; Miriam Cnop
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-08-31
Journal Detail:
Title:  Diabetes     Volume:  58     ISSN:  1939-327X     ISO Abbreviation:  Diabetes     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2009-11-26     Completed Date:  2009-12-14     Revised Date:  2013-03-19    
Medline Journal Info:
Nlm Unique ID:  0372763     Medline TA:  Diabetes     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2851-62     Citation Subset:  AIM; IM    
Affiliation:
Laboratory of Experimental Medicine, Université Libre de Bruxelles, Brussels, Belgium.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigens, Differentiation / metabolism
Apoptosis
Blotting, Western
Cell Survival
DNA-Binding Proteins / metabolism
Diabetes Mellitus, Type 2 / metabolism*,  prevention & control
Endoplasmic Reticulum / metabolism*
Forskolin / pharmacology
Glucagon-Like Peptide 1 / agonists*,  metabolism*
Heat-Shock Proteins / genetics,  metabolism*
Hypoglycemic Agents / pharmacology
Insulin-Secreting Cells / metabolism*
Lipid Metabolism* / drug effects
Male
Peptides / pharmacology
Polymerase Chain Reaction
Proto-Oncogene Proteins / metabolism
Proto-Oncogene Proteins c-jun / genetics,  metabolism*
RNA Interference
Rats
Rats, Wistar
Receptors, Glucagon / metabolism
Transcription Factors / metabolism
Up-Regulation
Venoms / pharmacology
Chemical
Reg. No./Substance:
0/Antigens, Differentiation; 0/DNA-Binding Proteins; 0/Heat-Shock Proteins; 0/Hspa5 protein, rat; 0/Hypoglycemic Agents; 0/Myd116 protein, rat; 0/Peptides; 0/Proto-Oncogene Proteins; 0/Proto-Oncogene Proteins c-jun; 0/Receptors, Glucagon; 0/Transcription Factors; 0/Venoms; 0/glucagon-like peptide-1 receptor; 0/regulatory factor X transcription factors; 141732-76-5/exenatide; 66428-89-5/Forskolin; 89750-14-1/Glucagon-Like Peptide 1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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