Chronic high glucose induced INS-1β cell mitochondrial dysfunction: A comparative mitochondrial proteome with SILAC

Xiulan Chen, Ziyou Cui, Shasha Wei, Junjie Hou, Zhensheng Xie, Xue Peng, Jing Li, Tanxi Cai, Haiying Hang, Fuquan Yang

Research output: Contribution to journalArticlepeer-review

15 Scopus citations

Abstract

As glucose-stimulated insulin secretion of pancreatic β cell is triggered and promoted by the metabolic messengers derived from mitochondria, mitochondria take a central stage in the normal function of β cells. β cells in diabetics were chronically exposed to hyperglycemia stimulation, which have been reported to exert deleterious effects on β-cell mitochondria. However, the mechanism of the toxic effects of hyperglycemia on β-cell mitochondria was not clear. In this study, we characterized the biological functional changes of rat INS-1β cells and their mitochondria with chronic exposure to hyperglycemia and created a research model of chronic hyperglycemia-induced dysfunctional β cells with damaged mitochondria. Then, SILAC-based quantitative proteomic approach was used to compare the mitochondrial protein expression from high glucose treated INS-1β cells and control cells. The expression of some mitochondrial proteins was found with significant changes. Functional classification revealed most of these proteins were related with oxidative phosphorylation, mitochondrial protein biosynthesis, substances metabolism, transport, and cell death. These results presented some useful information about the effect of glucotoxicity on the β-cell mitochondria.

Original languageEnglish (US)
Pages (from-to)3030-3039
Number of pages10
JournalProteomics
Volume13
Issue number20
DOIs
StatePublished - Oct 2013

Keywords

  • Cell biology
  • Diabetes
  • High glucose
  • Mitochondria
  • SILAC
  • β-Cell

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