Inhibition of Foxo1 Protects Pancreatic Islet β-Cells Against Fatty Acid and Endoplasmic Reticulum Stress–Induced Apoptosis
Author(s) -
Sara C. Martinez,
Katsuya Tanabe,
Corentin CrasMéneur,
Nada A. Abumrad,
Ernesto BernalMizrachi,
M. Alan Permutt
Publication year - 2008
Publication title -
diabetes
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.219
H-Index - 330
eISSN - 1939-327X
pISSN - 0012-1797
DOI - 10.2337/db07-0595
Subject(s) - foxo1 , unfolded protein response , endoplasmic reticulum , apoptosis , protein kinase b , fatty acid , endocrinology , kinase , medicine , biology , signal transduction , chemistry , microbiology and biotechnology , biochemistry
beta-Cells are particularly susceptible to fatty acid-induced apoptosis associated with decreased insulin receptor/phosphatidylinositol-3 kinase/Akt signaling and the activation of stress kinases. We examined the mechanism of fatty acid-induced apoptosis of mouse beta-cells especially as related to the role played by endoplasmic reticulum (ER) stress-induced Foxo1 activation and whether decreasing Foxo1 activity could enhance cell survival.
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