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Ceramide formation as a target in beta-cell survival and function.

Florian Lang1, Susanne Ullrich, Erich Gulbins

  • 1University of Tübingen, Institute of Physiology, Germany. florian.lang@uni-tuebingen.de

Expert Opinion on Therapeutic Targets
|June 4, 2011
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Summary

Ceramide contributes to beta-cell dysfunction and apoptosis, impacting insulin secretion. Inhibiting ceramide synthesis may protect beta-cells, offering therapeutic potential for metabolic disorders.

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Area of Science:

  • Endocrinology
  • Cell Biology
  • Metabolic Research

Background:

  • Ceramide is synthesized de novo or from sphingomyelin hydrolysis.
  • Ceramide plays a critical role in cellular signaling and stress responses.

Purpose of the Study:

  • To investigate the role of ceramide in beta-cell apoptosis, lipotoxicity, and amyloid-induced cell death.
  • To explore ceramide-sensitive signaling pathways and ion channel involvement in beta-cell function.

Main Methods:

  • Examined ceramide's impact on beta-cell apoptosis under various stress conditions (cytokines, amyloid, lipotoxicity).
  • Investigated the effects of genetic manipulation (sphingomyelin synthase 1 knockout) and pharmacological interventions (ceramidase, ceramide synthetase inhibition) on beta-cell function and survival.
  • Analyzed ceramide-mediated signaling pathways, including ER stress, mitochondrial dysfunction, and specific kinase/phosphatase activations.
  • Assessed ceramide's effect on ion channel activity in insulin-secreting cells.

Main Results:

  • Ceramide promotes beta-cell dysfunction and apoptosis induced by TNFα, IL-1β, IFN-γ, amyloid, and lipotoxicity.
  • Sphingomyelin synthase 1 knockout impairs insulin secretion; ceramidase inhibition or ceramide synthetase inhibition protects beta-cells from apoptosis.
  • Ceramide triggers ER stress, reduces mitochondrial membrane potential, and facilitates cytochrome c release, initiating apoptosis.
  • Ceramide signaling involves ERK1/2 activation, PASK downregulation, PP2A activation, NADPH oxidase stimulation, and reduced Kv-channel activity.

Conclusions:

  • Ceramide is a key mediator of beta-cell apoptosis and dysfunction in response to various insults.
  • Modulating ceramide metabolism through inhibition of ceramide synthetase or sphingomyelinase presents a potential therapeutic strategy for preserving beta-cell function and survival.