Department of Surgery, University of California, Irvine, CA 92697, USA.
Department of Medicine, University of California, Irvine, CA 92697, USA.
Int J Mol Sci. 2021 Feb 3;22(4):1509. doi: 10.3390/ijms22041509.
Diabetes is a chronic metabolic disorder characterized by inappropriately elevated glucose levels as a result of impaired pancreatic β cell function and insulin resistance. Extensive studies have been conducted to elucidate the mechanism involved in the development of β cell failure and death under diabetic conditions such as hyperglycemia, hyperlipidemia, and inflammation. Of the plethora of proposed mechanisms, endoplasmic reticulum (ER) stress, mitochondrial dysfunction, and oxidative stress have been shown to play a central role in promoting β cell dysfunction. It has become more evident in recent years that these 3 factors are closely interrelated and importantly aggravate each other. Oxidative stress in particular is of great interest to β cell health and survival as it has been shown that β cells exhibit lower antioxidative capacity. Therefore, this review will focus on discussing factors that contribute to the development of oxidative stress in pancreatic β cells and explore the downstream effects of oxidative stress on β cell function and health. Furthermore, antioxidative capacity of β cells to counteract these effects will be discussed along with new approaches focused on preserving β cells under oxidative conditions.
糖尿病是一种慢性代谢紊乱疾病,其特征是由于胰腺β细胞功能障碍和胰岛素抵抗导致血糖水平异常升高。大量研究已经阐明了在高血糖、高血脂和炎症等糖尿病条件下β细胞衰竭和死亡的发生机制。在众多提出的机制中,内质网(ER)应激、线粒体功能障碍和氧化应激被证明在促进β细胞功能障碍方面发挥着核心作用。近年来,越来越明显的是,这 3 个因素密切相关,并相互重要加重。氧化应激特别引起β细胞健康和存活的关注,因为已经表明β细胞表现出较低的抗氧化能力。因此,本综述将重点讨论导致胰腺β细胞氧化应激发展的因素,并探讨氧化应激对β细胞功能和健康的下游影响。此外,还将讨论β细胞的抗氧化能力以对抗这些影响,以及专注于在氧化条件下保护β细胞的新方法。