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Gestational hyperglycaemia impact on fetus health, and postpartum care

Aims: Previous studies have reported the induction of the viperin in isolated human islets exposed to proinflammatory cytokines and coxsackieviruses, as well as in the serum of people at risk of type 1 diabetes. We hypothesised that viperin plays a role in beta cell apoptosis during the development of type 1 diabetes. This project aimed to investigate the role of viperin in cytokinemediated beta cell apoptosis. Methods: siRNA knockdown of viperin was performed in INS1 cells followed by an assessment of gene expression and beta cell apoptosis. Apoptosis was also studied in islets isolated from viperin knockout (Rsad2KO) and control mice. Results: In INS1 cells and isolated wildtype mouse islets, viperin mRNA expression was highly induced within a few hours of exposure to proinflammatory cytokines, and expression levels decreased over time. Interestingly, apoptosis starts to peak as viperin levels decreased. siRNA knockdown of viperin in INS1 cells resulted in increased cytokineinduced apoptosis compared to siRNA controls (3.5fold increase with cytokines in siViperin cells; 1.5fold increase with cytokines in siControl cells; p < 0.0001 by ttest; n = 13). Similarly, cytokineinduced apoptosis was increased in isolated islets of Rsad2KO mice compared to wildtype controls (3.5fold increase with cytokine treatment of Rsad2KO islets; 2.5fold increase with cytokine treatment of wildtype islets; p < 0.05 by ttest; n = 12). RTqPCR revealed that viperin influenced the expression of cytokineresponse genes including NFkb, JAK2 and STAT1, and the ER stress marker CHOP (DDIT3). Conclusion: Our data indicate that viperin expression plays a protective role against cytokinemediated beta cell apoptosis.