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Abstract
Although several reports suggest a potentially deleterious role of macrophage migration inhibitory factor (MIF) in type 2 diabetes (T2D) pathology, it is still unclear how this pro-inflammatory cytokine acts on pancreatic beta cells. The aim of the present study was to evaluate MIF effects on murine beta cells in the in vitro settings mimicking T2D-associated conditions. Results indicate that recombinant MIF further increased apoptosis of pancreatic islets or MIN6 cells upon exposure to palmitic acid or glucose. This was accompanied by upregulation of several pro-apoptotic molecules. Furthermore, MIF potentiated nutrient-induced islet cell dysfunction, as revealed by lower glucose oxidation rate, ATP content, and depolarized mitochondrial membrane. The final outcome was potentiation of mitochondrial apoptotic pathway. The observed upregulation of nutrient-induced islet cell dysfunction and apoptosis by MIF implicates that silencing MIF may be beneficial for maintaining integrity of endocrine pancreas in obesity-associated T2D.
Acknowledgments
This work was supported by EASD/AstraZeneca Young Investigator Award and partly by the Project of Ministry of Education and Science, Republic of Serbia (No.: 173013). The excellent technical assistance of Ing-Britt Hallgren and Astrid Nordin (Department of Medical Cell Biology, Uppsala University, Sweden) is appreciated. The authors thank Drs Anders Tengholm (Department of Medical Cell Biology, Uppsala University, Sweden) and Junichi Miyazaki (Osaka University Graduate School of Medicine, Osaka, Japan) for generously providing them with MIN6 cells.
Declaration of interest : The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.