Source:http://linkedlifedata.com/resource/pubmed/id/12849705
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3-4
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pubmed:dateCreated |
2003-7-9
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pubmed:abstractText |
The aim of the present study was to investigate the effect of hypoglycaemia on the production capacity of the proinflammatory cytokines tumour necrosis factor-alpha (TNFalpha) and interleukin-1beta (IL-1beta) in subjects with and without diabetes. Hyperinsulinaemic (360 pmolm(-2) x min(-1)) stepped hypoglycaemic (5.0-3.5-2.5 mmoll(-1)) glucose clamps were performed in eight diabetic patients and in six non-diabetic subjects, and hyperinsulinaemic normoglycaemia (5.0 mmoll(-1)) control experiments were performed in four non-diabetic subjects. Circulating levels of cytokines and endotoxin-induced production of TNFalpha, IL-1beta, IL-6, and IL-10 were assessed. The effects of insulin and adrenaline were measured in separate in vitro experiments. In non-diabetic subjects, hypoglycaemia downregulated the production capacity of TNFalpha in a concentration-dependent fashion (P=0.007), but not of IL-1beta, IL-6, or IL-10. Compared to controls, the production capacity of TNFalpha in diabetic patients was already suppressed at normoglycaemia (P=0.02) and only fell in response to hypoglycaemic nadir (P=0.04). The downregulation of TNFalpha could not be explained by increased insulin or adrenaline levels. We conclude that hypoglycaemia specifically downregulates TNFalpha production capacity. Diabetic patients already have a suppressed TNFalpha production capacity at non-hypoglycaemic levels.
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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/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
1043-4666
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
22
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
71-6
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:12849705-Adult,
pubmed-meshheading:12849705-Cells, Cultured,
pubmed-meshheading:12849705-Dose-Response Relationship, Drug,
pubmed-meshheading:12849705-Down-Regulation,
pubmed-meshheading:12849705-Female,
pubmed-meshheading:12849705-Humans,
pubmed-meshheading:12849705-Hypoglycemia,
pubmed-meshheading:12849705-Insulin,
pubmed-meshheading:12849705-Interleukin-1,
pubmed-meshheading:12849705-Interleukin-10,
pubmed-meshheading:12849705-Interleukin-6,
pubmed-meshheading:12849705-Lipopolysaccharides,
pubmed-meshheading:12849705-Male,
pubmed-meshheading:12849705-Middle Aged,
pubmed-meshheading:12849705-Tumor Necrosis Factor-alpha
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pubmed:year |
2003
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pubmed:articleTitle |
Hypoglycaemia downregulates endotoxin-induced production of tumour necrosis factor-alpha, but does not affect IL-1beta, IL-6, or IL-10.
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pubmed:affiliation |
Department of General Internal Medicine, University Medical Center Nijmegen, Nijmegen, The Netherlands.
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pubmed:publicationType |
Journal Article
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