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Endocr Res. 2013;38(1):40-7. doi: 10.3109/07435800.2012.713423. Epub 2012 Aug 22.

Exendin-4 protects murine pancreatic β-cells from free fatty acid-induced apoptosis through PI-3K signaling.

Author information

1
Department of Endocrinology, Fujian Institute of Endocrinology, Union Hospital of Fujian Medical University, Fuzhou, Fujian, People's Republic of China.

Abstract

INTRODUCTION:

Glucagon-like peptide-1 (GLP-1) is an incretin hormone secreted by the L-cells of the distal intestine that has proliferative and anti-apoptotic actions on the β-cell.

METHODS:

In this study, exendin-4, a long-acting GLP-1 receptor agonist, was studied as a novel agent to suppress apoptosis in pancreatic β-cells and to protect against free fatty acid (FFA)-induced cytotoxicity.

RESULTS:

Exendin-4 significantly reduced the percentage of cells that underwent apoptosis when β-cells were exposed to FFA. Exendin-4 increased the levels of P-Akt and Bcl-2 proteins in FFA-induced β-cells, and this effect was blocked by Wortmannin.

CONCLUSIONS:

These results suggest that phosphoinositide-3 kinase signaling is involved in the modulation of β-cell apoptosis which is induced by exendin-4. Taken together, our findings provide a new mechanism for the modulation of exendin-4 in the pathological processes underlying FFA-induced diabetes mellitus.

PMID:
22913774
DOI:
10.3109/07435800.2012.713423
[Indexed for MEDLINE]

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