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Macrophage migration inhibitory factor (MIF) enhances palmitic acid- and glucose-induced murine beta cell dysfunction and destruction in vitro.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
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2012 (English)In: Growth Factors, ISSN 0897-7194, E-ISSN 1029-2292, Vol. 30, no 6, 385-393 p.Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
2012. Vol. 30, no 6, 385-393 p.
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Immunology in the medical area
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URN: urn:nbn:se:uu:diva-190890DOI: 10.3109/08977194.2012.734506ISI: 000312222900003PubMedID: 23137174OAI: oai:DiVA.org:uu-190890DiVA: diva2:584391
Available from: 2013-01-09 Created: 2013-01-09 Last updated: 2017-12-06Bibliographically approved

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Sandler, Stellan

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