Protein Tyrosine Phosphatase-1B Modulates Pancreatic β-cell Mass

Pancreatic Islets
DOI: 10.1371/journal.pone.0090344 Publication Date: 2014-02-28T22:09:13Z
ABSTRACT
Protein tyrosine phosphatase 1B (PTP1B) is a negative regulator of the insulin signalling pathway. It has been demonstrated that PTP1B deletion protects against development obesity and Type 2 Diabetes, mainly through its action on peripheral tissues. However, little attention paid to role in β-cells. Therefore, our aim was study pancreatic Silencing expression β-cell line (MIN6 cells) reveals significance this endoplasmic reticulum bound regulation cell proliferation apoptosis. Furthermore, ablation able regulate key proteins involved and/or apoptosis pathways, such as STAT3, AKT, ERK1/2 p53 isolated islets from knockout (PTP1B −/−) mice. Morphometric analysis −/− mice showed higher area, concomitantly with lower when compared their respective wild type (WT) littermates. At functional level, 8 weeks old exhibit enhanced glucose-stimulated secretion. Moreover, were partially reverse streptozotocin-induced loss. Together, data highlight for first time involvement physiology, reinforcing potential therapeutical target treatment failure, central aspect pathogenesis Diabetes.
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