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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1995-6-12
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pubmed:abstractText |
Since copper [Cu(II)] is a necessary cofactor for both intra-mitochondrial enzymes involved in energy production and hydroxyl scavenger enzymes, two hypothesised mechanisms for action of interleukin-I beta (IL-1 beta), we studied whether Cu(II) addition could prevent the inhibitory effect of IL-1 beta on insulin release and glucose oxidation in rat pancreatic islets. Islets were incubated with or without 50 U/ml IL-1 beta, in the presence or absence of various concentrations of Cu(II)-GHL (Cu(II) complexed with glycyl-L-histidyl-L-lysine, a tripeptide known to enhance copper uptake into cultured cells). CuSO4 (1-1000 ng/ml) was used as a control for Cu(II) effect when present as an inorganic salt. At the end of the incubation period, insulin secretion was evaluated in the presence of either 2.8 mmol/l (basal insulin secretion) or 16.7 mmol/l glucose (glucose-induced release). In control islets basal insulin secretion was 92.0 +/- 11.4 pg.islet-1 h-1 (mean +/- SEM, n = 7) and glucose-induced release was 2824.0 +/- 249.0 pg.islet-1 h-1. In islets pre-exposed to 50 U/ml IL-1 beta, basal insulin release was not significantly affected but glucose-induced insulin release was greatly reduced (841.2 +/- 76.9, n = 7, p < 0.005). In islets incubated with IL-1 beta and Cu-GHL (0.4 mumol/l, maximal effect) basal secretion was 119.0 +/- 13.1 pg.islet-1 h-1 and glucose-induced release was 2797.2 +/- 242.2, (n = 7, p < 0.01 in respect to islets exposed to IL-1 beta alone).(ABSTRACT TRUNCATED AT 250 WORDS)
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Copper,
http://linkedlifedata.com/resource/pubmed/chemical/Copper Sulfate,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Oligopeptides,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Superoxide Dismutase,
http://linkedlifedata.com/resource/pubmed/chemical/glycyl-histidyl-lysine
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0012-186X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
38
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
39-45
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:7744228-Animals,
pubmed-meshheading:7744228-Cells, Cultured,
pubmed-meshheading:7744228-Copper,
pubmed-meshheading:7744228-Copper Sulfate,
pubmed-meshheading:7744228-Glucose,
pubmed-meshheading:7744228-Insulin,
pubmed-meshheading:7744228-Interleukin-1,
pubmed-meshheading:7744228-Islets of Langerhans,
pubmed-meshheading:7744228-Male,
pubmed-meshheading:7744228-Nitric Oxide,
pubmed-meshheading:7744228-Oligopeptides,
pubmed-meshheading:7744228-Oxidation-Reduction,
pubmed-meshheading:7744228-Rats,
pubmed-meshheading:7744228-Rats, Wistar,
pubmed-meshheading:7744228-Recombinant Proteins,
pubmed-meshheading:7744228-Superoxide Dismutase
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pubmed:year |
1995
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pubmed:articleTitle |
Copper addition prevents the inhibitory effects of interleukin 1-beta on rat pancreatic islets.
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pubmed:affiliation |
Institute of Internal Medicine, Metabolism and Endocrinology, University of Catania Medical School, Italy.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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