Nicotinamide Inhibits IRF-1 mRNA Induction and Prevents IL-1β-Induced Nitric Oxide Synthase Expression in Pancreatic β Cells

Atsuya Akabane, Ichiro Kato, Shin Takasawa, Michiaki Unno, Hideto Yonekura, Takashi Yoshimoto, Hiroshi Okamoto

Research output: Contribution to journalArticlepeer-review

30 Citations (Scopus)

Abstract

Nitric oxide produced by inducible nitric oxide synthase in islets exerts inhibitory and cytotoxic effects on pancreatic β cells and is therefore thought to be a potent mediator in the pathogenesis of Type I diabetes mellitus. Here, using isolated rat pancreatic islets, we show that high-concentration nicotinamide (20 mM), but not low-concentration nicotinamide (5 mM) attenuates the interleukin-1β-evoked inhibition of glucose-induced insulin secretion by preventing the induction of interferon regulatory factor-1, a transcriptional factor which plays an essential role in inducible nitric oxide synthase gene expression, and the interleukin-1β-induced nitric oxide formation. High-concentration nicotinamide also restored an interleukin-1β-induced decrease in ATP content in pancreatic β cells, suggesting that interleukin-1β-induced nitric oxide inhibits the mitochondrial function. The present results show the molecular basis of the preventive effect of high-dose nicotinamide on Type I diabetes mellitus.

Original languageEnglish
Pages (from-to)524-530
Number of pages7
JournalBiochemical and biophysical research communications
Volume215
Issue number2
DOIs
Publication statusPublished - 1995 Jan 1

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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