IL-34 causes inflammation and beta cell apoptosis and dysfunction in gestational diabetes mellitus. Issue 11 (November 2019)

• Record Type: Journal Article
• Authors: Piao, Chenghao; Wang, Xiaojie; Peng, Shiqiao; Guo, Xinyu; Zhao, Hui; He, Li; Zeng, Yan; Zhang, Fan; Zhu, Kewen; Wang, Yiwei
• Is Part Of: Endocrine connections. Volume 8:Issue 11(2019)
• Page Start: 1503
• Page End: 1512
• Publication Date: 2019-11
• Subjects: gestational diabetes mellitus -- IL-34 -- CSF-1R -- apoptosis -- pancreatic β cell; Endocrinology -- Periodicals; 616.4005
• DOI: 10.1530/EC-19-0436
• Languages: English
• ISSNs: 2049-3614

Abstract

Abstract : Objective: Gestational diabetes mellitus (GDM) is characterized by glucose intolerance during gestation. It is associated with a series of maternal and foetal complications. Interleukin (IL)-34 is a recently discovered pro-inflammatory cytokine that functions as a ligand for colony-stimulating factor-1 receptor (CSF-1R). The contribution of IL-34 in the development of multiple chronic inflammatory diseases and autoimmune diseases has been recently discovered. The aim of this study was to evaluate whether IL-34 participates in the pathogenesis of GDM. Method: A total of 120 women were enrolled in this study, which included 60 GDM patients and age- and sex-matched healthy pregnant women. The expression of IL-34 in serum, cord blood and placental tissues was analysed by ELISA and Western blot assays. The association between IL-34 levels and clinical features was also studied. We additionally evaluated the effect of recombinant mouse IL-34 (rmIL-34) on apoptosis and pancreatic β cell function. Results: We found that IL-34 expression is highly increased in serum, cord blood and placental tissues in patients with GDM. In addition, there was a positive association between serum IL-34 and insulin resistance and glucose concentrations. Our data also revealed that IL-34 contributes to the apoptosis of pancreatic β cells in GDM caused by CSF-1R. Furthermore, functional studies found that IL-34 inhibited pancreatic β cell function and cell viability, while CSF-1R inhibitor blocked this effect. Conclusion: IL-34 plays a crucial role in the development of GDM by targeting CSF-1R, insulin production and β cell function.