Glucagon-like peptide-1 agonists protect pancreatic beta-cells from lipotoxic endoplasmic reticulum stress through upregulation of BiP and JunB

Autor: Daniel Andrade Da Cunha, Piero Marchetti, Mariana Igoillo-Esteve, Fernanda Ortis, Roberto Lupi, Laurence Ladrière, Esteban Nicolas Gurzov, Decio L. Eizirik, Miriam Cnop
Jazyk: angličtina
Rok vydání: 2009
Předmět:
Male
Proto-Oncogene Proteins c-jun
Endocrinology
Diabetes and Metabolism
Biologie générale
Apoptosis
Endoplasmic Reticulum
Polymerase Chain Reaction
Salubrinal
chemistry.chemical_compound
Glucagon-Like Peptide 1
Insulin-Secreting Cells
Receptors
Glucagon
Venoms -- pharmacology
Heat-Shock Proteins
Transcription Factors -- metabolism
Forskolin
Endoplasmic Reticulum -- metabolism
Sciences bio-médicales et agricoles
Cell biology
Up-Regulation
DNA-Binding Proteins
Receptors
Glucagon -- metabolism
Original Article
RNA Interference
Signal transduction
Biologie
DNA-Binding Proteins -- metabolism
Antigens
Differentiation -- metabolism
endocrine system
medicine.medical_specialty
JUNB
Cell Survival
Hypoglycemic Agents -- pharmacology
Blotting
Western
Regulatory Factor X Transcription Factors
Diabetes Mellitus
Type 2 -- metabolism -- prevention & control
Peptides -- pharmacology
Biology
Inhibitor of apoptosis
Glucagon-Like Peptide-1 Receptor
Proto-Oncogene Proteins c-jun -- genetics -- metabolism
Downregulation and upregulation
Proto-Oncogene Proteins
Internal medicine
Internal Medicine
medicine
Hypoglycemic Agents
Animals
Heat-Shock Proteins -- genetics -- metabolism
Colforsin -- pharmacology
Rats
Wistar
Diabétologie
Venoms
Endoplasmic reticulum
Colforsin
Glucagon-Like Peptide 1 -- agonists -- metabolism
Biologie moléculaire
Lipid Metabolism -- drug effects
Enseignement des sciences
Lipid Metabolism
Antigens
Differentiation
Rats
Proto-Oncogene Proteins -- metabolism
Endocrinology
Diabetes Mellitus
Type 2
Islet Studies
chemistry
Insulin-Secreting Cells -- metabolism
Unfolded protein response
Exenatide
Biologie cellulaire
Peptides
Transcription Factors
Zdroj: Diabetes (New York, N.Y.), 58 (12
Diabetes
Popis: 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.
info:eu-repo/semantics/published
Databáze: OpenAIRE
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