Activation of Peroxisome Proliferator-Activated Receptor-γ by Rosiglitazone Protects Human Islet Cells against Human Islet Amyloid Polypeptide Toxicity by a Phosphatidylinositol 3′-Kinase-Dependent Pathway | Zendy

ChiaYu Lin | Zendy; Tatyana Gurlo | Zendy; Leena Haataja | Zendy; Willa A. Hsueh | Zendy; Peter C. Butler | Zendy

Open Access

Activation of Peroxisome Proliferator-Activated Receptor-γ by Rosiglitazone Protects Human Islet Cells against Human Islet Amyloid Polypeptide Toxicity by a Phosphatidylinositol 3′-Kinase-Dependent Pathway

Author(s) -

ChiaYu Lin,

Tatyana Gurlo,

Leena Haataja,

Willa A. Hsueh,

Peter C. Butler

Publication year - 2005

Publication title -

the journal of clinical endocrinology and metabolism

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.206

H-Index - 353

eISSN - 1945-7197

pISSN - 0021-972X

DOI - 10.1210/jc.2005-0079

Subject(s) - islet , rosiglitazone , amyloid (mycology) , apoptosis , endocrinology , peroxisome proliferator activated receptor gamma , receptor , peroxisome proliferator activated receptor , peroxisome , chemistry , medicine , phosphatidylinositol , microbiology and biotechnology , cancer research , kinase , biology , diabetes mellitus , biochemistry , inorganic chemistry

Type 2 diabetes mellitus (T2DM) is characterized by a deficit in beta-cell mass, increased beta-cell apoptosis, and islet amyloid derived from islet amyloid polypeptide (IAPP). Human IAPP (h-IAPP) applied to beta-cells forms toxic oligomers that induce apoptosis. Thiazolidinediones, ligands of peroxisome proliferator-activated receptor-gamma (PPAR-gamma), can delay the onset of T2DM.

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