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Journal of Diabetes Research
Volume 2016, Article ID 7592931, 6 pages
Research Article

IL-6 Promotes Islet β-Cell Dysfunction in Rat Collagen-Induced Arthritis

1Department of Rheumatology, Jiangxi Provincial People’s Hospital, Nanchang 330006, China
2Department of Critical Care Medicine, The First Affiliated Hospital of Xiamen University, Xiamen 361003, China

Received 21 July 2016; Revised 10 October 2016; Accepted 23 October 2016

Academic Editor: Jixin Zhong

Copyright © 2016 Huan Jin et al. 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.


The aim of this study was to explore the possible mechanism of rheumatoid arthritis- (RA-) related abnormal glucose metabolism. The model of collagen-induced arthritis (CIA) was established by intradermal injection of type II collagen into Wistar rats; complete Freund’s adjuvant injections were used as the control group. Fasting plasma glucose (FBG) was measured by the glucose oxidase method. Fasting insulin (FIns) and the expressions of IL-6 were detected by ELISA. Islet caspase-3 was examined by immunohistochemistry. On day 17 after immunization, FBG of the CIA group showed an elevated FBG value compared with the control group. Meanwhile, the FIns of group CIA was lower when compared with the control group. Interestingly, the inflammatory cytokine IL-6 expression was significantly increased when compared with the control group. As expected, the abnormal glucose metabolism was accompanied by the increased IL-6 expression. Furthermore, in line with the upregulated IL-6 expression, the apoptosis related enzyme caspase-3 was also markedly increased. These data showed that the elevated FBG in CIA may be associated with the reduced FIns level secondary to the overapoptosis of pancreas islet cells induced by IL-6.