Abstract
Aims
The preservation of pancreatic β-cell function is a key point in the treatment of type 2 diabetes mellitus. There is substantial evidence demonstrating that heat-shock protein 90 (Hsp90) is needed for the stabilization and correct folding of client proteins and plays important roles in various biological processes. Here, we revealed the important role of Hsp90 in β-cell function.
Methods
Islets from male Sprague–Dawley rats were isolated to be used for further RT-PCR, Western blot, and insulin secretion test ex vivo in response to different stimuli.
Results
Our results revealed that Hsp90 expression was significantly decreased in isolated rat islets exposed to high glucose, which was involved in glucokinase activation and glucose metabolism, not calcium signaling. Two kinds of Hsp90 inhibitors 17-DMAG and CCT018159 markedly enhanced glucose-stimulated insulin secretion from rat islets, along with increased expressions of genes closely related to β-cell function.
Conclusions
These data indicate that Hsp90 may be involved in high glucose-induced islet function adaptation.
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Acknowledgments
This work was funded by grants from the National Natural Science Foundation of China (81170720, 81270910, 81370876, 81471030, and 81570693).
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All experimental procedures related to animal handling in the present study were adhered to the approval obtained from the Laboratory Animal Ethics Committee of Ruijin Hospital.
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This article does not contain any studies with human subjects performed by any of the authors. All institutional and national guidelines for the care and use of laboratory animals were followed.
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Xue Yang and Yuqing Zhang have contributed equally to this work.
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Yang, X., Zhang, Y., Xu, W. et al. Potential role of Hsp90 in rat islet function under the condition of high glucose. Acta Diabetol 53, 621–628 (2016). https://doi.org/10.1007/s00592-016-0852-2
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DOI: https://doi.org/10.1007/s00592-016-0852-2