Ceramide inhibits pancreatic β‐cell insulin production and mitogenesis and mimics the actions of interleukin‐1β
- 3 July 1995
- journal article
- Published by Wiley in FEBS Letters
- Vol. 367 (3) , 283-286
- https://doi.org/10.1016/0014-5793(95)00470-t
Abstract
Ceramide, generated during sphingomyelinase-induced sphingolipid cleavage, is considered an important mediator in cytokine signaling. The effects of endogenously generated and exogenously delivered ceramide on long-term insulin secretion and replication by pancreatic beta-cells were investigated, and compared to the effects of interleukin 1 beta (IL-1 beta). Generation of beta-cell ceramide by exogenous sphingomyelinase, or addition of cell-permeant ceramide analogs C2-ceramide and C6-ceramide, caused inhibitor effects on beta-cell insulin production and mitogenesis mimicing those evoked by IL-1 beta. Hence, ceramide may be involved in transducing the cytostatic and cytotoxic actions of IL-1 beta in the beta-cell.Keywords
This publication has 28 references indexed in Scilit:
- Interleukin-1β-Induced Nitric Oxide Production Activates Apoptosis in Pancreatic RINm5F CellsExperimental Cell Research, 1994
- The sphingomyelin pathway in tumor necrosis factor and interleukin-1 signalingPublished by Elsevier ,1994
- Characterization of serine/threonine protein phosphatases in RINm5F insulinoma cellsBioscience Reports, 1993
- Programmed Cell Death Induced by CeramideScience, 1993
- Activation of the Sphingomyelin Signaling Pathway in Intact EL4 Cells and in a Cell-Free System By IL-1βScience, 1993
- Intracellular Signaling by Hydrolysis of Phospholipids and Activation of Protein Kinase CScience, 1992
- Intracellular signal transduction pathways that control pancreatic β‐cell proliferationFEBS Letters, 1992
- Phorbol ester stimulation of pancreatic β‐cell replication, polyamine content and insulin secretionFEBS Letters, 1991
- Inhibition of fetal rat pancreatic β‐cell replication by interleukin‐1β in vitro is not mediated through pertussis toxin‐sensitive G‐proteins, a decrease in cyclic AMP, or protease activationFEBS Letters, 1991
- Determination of total serum insulin (IRI) in insulin-treated diabetic patientsDiabetologia, 1972