SIRT6 protects against palmitateinduced pancreatic β-cell dysfunction and apoptosis

Xiwen Xiong, Xupeng Sun, Qingzhi Wang, Xinlai Qian, Yang Zhang, Xiaoyan Pan, X. Charlie Dong

Research output: Contribution to journalArticle

16 Scopus citations


Chronic exposure of pancreatic β-cells to abnormally elevated levels of free fatty acids can lead to β-cell dysfunction and even apoptosis, contributing to type 2 diabetes pathogenesis. In pancreatic β-cells, sirtuin 6 (SIRT6) has been shown to regulate insulin secretion in response to glucose stimulation. However, the roles played by SIRT6 in β-cells in response to lipotoxicity remain poorly understood. Our data indicated that SIRT6 protein and mRNA levels were reduced in islets from diabetic and aged mice. High concentrations of palmitate (PA) also led to a decrease in SIRT6 expression in MIN6 β-cells and resulted in cell dysfunction and apoptosis. Knockdown of Sirt6 caused an increase in cell apoptosis and impairment in insulin secretion in response to glucose in MIN6 cells even in the absence of PA exposure. Furthermore, overexpression of SIRT6 alleviated the palmitate-induced lipotoxicity with improved cell viability and increased glucose-stimulated insulin secretion. In summary, our data suggest that SIRT6 can protect against palmitate-induced β-cell dysfunction and apoptosis.

Original languageEnglish (US)
Pages (from-to)159-165
Number of pages7
JournalJournal of Endocrinology
Issue number2
StatePublished - 2016


  • Apoptosis
  • Insulin secretion
  • Palmitate
  • Sirtuin 6
  • mIN6 cells

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

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