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Xiang Kong [1; 2; 3] and Ai-Ling Lu [4] and Xin-Ming Yao [2] and Qiang Hua [2] and Xiao-Yong Li [1] and Li Qin [1] and Hong-Mei Zhang [1] and Guang-Xun Meng [4] and Qing Su [1]

Academic Editor: Izabela Sadowska-Bartosz

1, Department of Endocrinology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200092, China, shsmu.edu.cn

2, Department of Endocrinology, The First Affiliated Hospital of Wannan Medical College, Yijishan Hospital, Wuhu 241001, China, wnmc.edu.cn

3, Engineering Technology Research Center of Polysaccharides Drug, Wuhu, Anhui Province 241002, China

4, Key Laboratory of Molecular Virology & Immunology, Institut Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China, cas.cn

Received May 16, 2017; Revised Aug 5, 2017; Accepted Aug 29, 2017

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

1. Introduction

Advanced glycation end products (AGEs) are generated nonenzymatically, and the formation of AGEs is greatly accelerated by prolonged hyperglycemia in patients with diabetes mellitus (DM) [1, 2]. AGE accumulation is one of the main factors that contribute to ageing and is an important element of etiopathology of age-related diseases, especially type 2 DM and its complications [3–5]. Recent studies have pointed out that AGE accumulation directly causes insulin-producing β-cell dysfunction and apoptosis in vivo [6–9]. These effects are attributed, at least in part, to an increase in cellular reactive oxygen species (ROS) production. Nonetheless, the precise role of AGE-mediated ROS release in β-cell damage remains unclear.

Inflammation is a critical mechanism leading to β-cell dysfunction and death, wherein the inflammatory cytokines play an important role [10, 11]. Among the various proinflammatory cytokines, interleukin-1β (IL-1β) plays a major role in DM. Clinical studies reported that inhibition of IL-1β by either IL-1 receptor antagonist or IL-1β antibody in patients with type 2 DM leads to improvement in glycemia and β-cell function [12, 13]. It is known that IL-1β secretion is predominantly mediated by the cysteine protease caspase-1, which is mainly activated by inflammasomes, especially the nucleotide-binding domain leucine-rich repeat containing receptor, the pyrin domain-containing 3 (NLRP3) inflammasome [14].

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