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Pancreatic islet response to hyperglycemia is dependent on peroxisome proliferator‐activated receptor alpha (PPARα)
Author(s) -
Bihan Hélène,
Rouault Christine,
Reach Gérard,
Poitout Vincent,
Staels Bart,
Guerre-Millo Michèle
Publication year - 2005
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2005.03.020
Subject(s) - endocrinology , medicine , islet , peroxisome proliferator activated receptor , glucose homeostasis , insulin , peroxisome proliferator activated receptor alpha , biology , peroxisome , pancreatic islets , receptor , type 2 diabetes , insulin oscillation , rosiglitazone , diabetes mellitus , insulin resistance , nuclear receptor , transcription factor , biochemistry , gene
This study tests the hypothesis that islet peroxisome proliferator‐activated receptor alpha (PPARα) influences insulin secretion. Freshly isolated islets of normoglycemic PPARα‐null mice display no major alteration of glucose‐stimulated insulin release. However, after 24 h of culture in high glucose, PPARα‐null islets exhibit elevated basal insulin secretion and fail to increase insulin mRNA. 24‐h culture with palmitate replicates this phenotype in wild‐type islets. The data suggest that PPARα is needed to ensure appropriate insulin secretory response in situation of short‐term hyperglycemia, likely by maintaining islet lipid homeostasis. As such, islet PPARα could contribute to delay the progression of type 2 diabetes.