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Free Radic Biol Med. 2018 Aug 1;123:53-61. doi: 10.1016/j.freeradbiomed.2018.05.007. Epub 2018 May 9.

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

Author information

1
Department of Endocrinology, Peking University First Hospital, No. 8 Xi Shi Ku Street, Xi Cheng District, Beijing 100034, China.
2
Department of Endocrinology, Peking University First Hospital, No. 8 Xi Shi Ku Street, Xi Cheng District, Beijing 100034, China. Electronic address: junqing.zhang@pkufh.cn.
3
Division of Endocrinology, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA. Electronic address: li@email.chop.edu.
4
Laboratory of Electron Microscopy, Peking University First Hospital, Beijing 100034, China.

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 oxidative stress by increasing glycine transporter-1-mediated synthesis of GSH and by reducing glycine receptor-mediated ROS production.

KEYWORDS:

Glycine; Oxidative stress; Pancreatic β-cells; Streptozotocin (STZ)-induced diabetic rats

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