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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
2001-6-11
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pubmed:abstractText |
The cytokine interleukin-1 beta (IL-1 beta) is cytotoxic to rat pancreatic beta-cells and has been implicated in the pathogenesis of insulin-dependent diabetes mellitus. IL-1 beta causes expression of inducible nitric oxide synthase (iNOS) and production of nitric oxide (NO). NO may be the mediator of the cytotoxic effect of IL-1 beta in rat islets and beta-cell lines. Glucose has been shown to modulate the effects of IL-1 beta on accumulated insulin release and potentiate NO production in rat islets, but the biochemical mechanism is unknown. IL-1 beta activates the mitogen-activated protein kinases (MAPK) extracellular signal-regulated kinase 1 and 2 (ERK1/2), p38 and c-jun NH2-terminal kinase (JNK) in rat islets and beta-cells. Glucose may modulate MAPK activity although contrasting data have been published. The aim of this study was to investigate whether glucose potentiated IL-1 beta-induced p38 and ERK1/2 activity in rat islets. It was shown that glucose alone increased the phosphorylation of the MAPK substrates Elk-1 and activating transcription factor 2 (ATF2). D-glucose potentiated the p38 activity induced by a low concentration of IL-1 beta, whereas no effect was seen at high concentrations of IL-1 beta. Inhibition of p38 activity prevented IL-1 beta-induced nitrite production in the presence of D-glucose. We conclude that IL-1 beta-induced NO production in the presence of glucose is signalled by the p38 pathway.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Activating Transcription Factor 2,
http://linkedlifedata.com/resource/pubmed/chemical/Atf2 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP Response...,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Elk1 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Nitrites,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/ets-Domain Protein Elk-1,
http://linkedlifedata.com/resource/pubmed/chemical/p38 Mitogen-Activated Protein...
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pubmed:status |
MEDLINE
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pubmed:issn |
1148-5493
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
12
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
331-9
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:11399523-Activating Transcription Factor 2,
pubmed-meshheading:11399523-Animals,
pubmed-meshheading:11399523-Cyclic AMP Response Element-Binding Protein,
pubmed-meshheading:11399523-DNA-Binding Proteins,
pubmed-meshheading:11399523-Glucose,
pubmed-meshheading:11399523-Interleukin-1,
pubmed-meshheading:11399523-Islets of Langerhans,
pubmed-meshheading:11399523-Mitogen-Activated Protein Kinases,
pubmed-meshheading:11399523-Nitrites,
pubmed-meshheading:11399523-Phosphorylation,
pubmed-meshheading:11399523-Precipitin Tests,
pubmed-meshheading:11399523-Proto-Oncogene Proteins,
pubmed-meshheading:11399523-Rats,
pubmed-meshheading:11399523-Rats, Wistar,
pubmed-meshheading:11399523-Signal Transduction,
pubmed-meshheading:11399523-Substrate Specificity,
pubmed-meshheading:11399523-Transcription Factors,
pubmed-meshheading:11399523-ets-Domain Protein Elk-1,
pubmed-meshheading:11399523-p38 Mitogen-Activated Protein Kinases
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pubmed:articleTitle |
Glucose potentiates interleukin-1 beta (IL-1 beta)-induced p38 mitogen-activated protein kinase activity in rat pancreatic islets of Langerhans.
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pubmed:affiliation |
Steno Diabetes Center, 2 Niels Steensens vej, DK-2820 Gentofte, Denmark.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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