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Journal of Diabetes Research
Volume 2016 (2016), Article ID 9158562, 9 pages
Research Article

Islet Brain 1 Protects Insulin Producing Cells against Lipotoxicity

1Service of Internal Medicine, Centre Hospitalier Universitaire Vaudois and University of Lausanne, 1011 Lausanne, Switzerland
2University of Lille, European Genomic Institute for Diabetes (EGID) FR 3508, UMR CNRS 8199, Faculty of Medicine West, 1 place de Verdun, 59045 Lille, France
3Department of Pharmacology and the Alberta Diabetes Institute, University of Alberta, Edmonton, AB, Canada
4University of Lille, EGID FR 3508, Department of Endocrine Surgery, Lille University Hospital, UMR INSERM 1190, Lille, France
5Department of Molecular and Cellular Biochemistry, Ohio State University, 1060 Carmack Road, Columbus, OH, USA

Received 6 January 2015; Accepted 6 March 2015

Academic Editor: Li Chen

Copyright © 2016 Saška Brajkovic 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.


Chronic intake of saturated free fatty acids is associated with diabetes and may contribute to the impairment of functional beta cell mass. Mitogen activated protein kinase 8 interacting protein 1 also called islet brain 1 (IB1) is a candidate gene for diabetes that is required for beta cell survival and glucose-induced insulin secretion (GSIS). In this study we investigated whether IB1 expression is required for preserving beta cell survival and function in response to palmitate. Chronic exposure of MIN6 and isolated rat islets cells to palmitate led to reduction of the IB1 mRNA and protein content. Diminution of IB1 mRNA and protein level relied on the inducible cAMP early repressor activity and proteasome-mediated degradation, respectively. Suppression of IB1 level mimicked the harmful effects of palmitate on the beta cell survival and GSIS. Conversely, ectopic expression of IB1 counteracted the deleterious effects of palmitate on the beta cell survival and insulin secretion. These findings highlight the importance in preserving the IB1 content for protecting beta cell against lipotoxicity in diabetes.