High glucose triggers multiple cellular stress signaling in pancreatic β-cells and potentiate proinflammation and β-cell dysfunction
Abstract
Pancreatic β-cells are highly susceptible to high glucose-induced metabolic stress and β-cell dysfunction is emerging as an early event in the etiology of type 2 diabetes. The current study investigated the effects of high glucose-induced multiple cellular stress signaling that could promote proinflammation and β-cell dysfunction. The study also tested the effect of metformin, lactoferrin and tauroursodeoxycholic acid (TUDCA, an inhibitor of ER stress) in providing protection for β-cells.
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