Glycine Transporter-1 and glycine receptor mediate the antioxidant effect of glycine in diabetic rat islets and INS-1 cells

Free Radical Biology & Medicine
Lei ChenXiaohui Guo

Abstract

Oxidative stress is the main inducer of β-cell damage, which underlies the pathogenesis of diabetes. Evidence suggests that glycine, a recognized antioxidant, may improve β-cell function; however, its mechanism in protecting diabetic β-cells against oxidative stress has not been directly investigated. Using a streptozotocin-induced diabetic rat model and INS-1 pancreatic β-cells, we evaluated whether glycine can attenuate diabetic β-cell damage induced by oxidative stress. In diabetic rats, glycine stimulated insulin secretion; enhanced plasma glutathione (GSH), catalase and superoxide dismutase levels; reduced plasma 8-hydroxy-2 deoxyguanosine and islet p22phox levels; and improved islet β-cell mitochondrial degeneration and insulin granule degranulation. In INS-1 cells, glycine reduced the intracellular reactive oxygen species (ROS) concentration and inhibited apoptosis induced by high glucose or H2O2. Glycine transporter-1 inhibitor blocked the antioxidative effect of glycine by reducing the intracellular GSH content, and glycine receptor inhibitor reversed the glycine antioxidative effect by blocking p22phox. Collectively, our findings reveal a mechanism by which glycine protects diabetic β-cells against damage caused by ox...Continue Reading

Citations

Dec 12, 2019·Frontiers in Molecular Neuroscience·Rama Ashraf HusseinUlrike Breitinger
Jun 19, 2019·Nutrients·Anaïs AlvesBéatrice Morio
Dec 29, 2020·Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association·Yao LiuDaidi Fan
Jan 30, 2021·Frontiers in Cell and Developmental Biology·Zhen WeiPing Yi

❮ Previous
Next ❯

Related Concepts

Related Feeds

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis