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Müller, S.* ; Martin, S.* ; Koenig, W.* ; Hanifi-Moghaddam, P.* ; Rathmann, W.* ; Haastert, B.* ; Giani, G.* ; Illig, T. ; Thorand, B. ; Kolb, H.*

Impaired glucose tolerance is associated with increased serum concentrations of interleukin 6 and co-regulated acute-phase proteins but not TNF-alpha or its receptors.

Diabetologia 45, 805-812 (2002)
DOI
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Aims/hypothesis. A population-based sample was studied to define immune abnormalities in individuals at risk of Type II (non-insulin-dependent) diabetes mellitus because of impaired glucose tolerance. Methods. A total of 1653 individuals aged 55 to 74 years participated in a population based survey in Southern Germany (KORA Survey 2000). Those without a history of diabetes were subjected to an OGTT. Randomly selected subjects with IGT (n=80) were compared with non-diabetic control subjects (n=77) and patients with Type II diabetes (n=152) of the same population-based sample after matching for age and sex. Immune parameters were analysed in serum with rigidly evaluated ELISA. Results. Serum pro-inflammatory cytokine interleukin 6 (IL-6) concentrations were higher in subjects with IGT and Type II diabetes than in the control subjects (median 1.8 and 2.5 vs 0.8 pg/ml, p<0.0001). Soluble IL-6 receptors potentiate IL-6 bioactivity and their concentrations were mildly increased in Type II diabetes (p<0.05). These immune changes seem relevant because IL-6 dependent acute-phase proteins C-reactive protein, serum amyloid A protein and fibrinogen were also increased in IGT and Type II diabetes. Circulating concentrations of TNF-α and its two receptors sTNF-R60 and sTNF-R80 were not increased in IGT subjects compared with the control subjects. Conclusion/interpretation. Our study shows systemic up-regulation of selected inflammatory mediators in patients with Type II diabetes and IGT. The pattern observed is non-random and fits with an IL-6 associated rather than TNF-α associated response. Type II diabetes impaired glucose tolerance systemic inflammation interleukin 6 tumour necrosis factor α C-reactive protein serum amyloid A protein innate immunity cytokine acute-phase protein
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Type II diabetes; impaired glucose tolerance; systemic inflammation; interleukin 6; tumour necrosis factor alpha; C-reactive protein; serum amyloid A protein; innate immunity; cytokine; acute-phase protein
Sprache englisch
Veröffentlichungsjahr 2002
HGF-Berichtsjahr 0
ISSN (print) / ISBN 0012-186X
e-ISSN 1432-0428
Zeitschrift Diabetologia
Quellenangaben Band: 45, Heft: 6, Seiten: 805-812 Artikelnummer: , Supplement: ,
Verlag Springer
Verlagsort Berlin ; Heidelberg [u.a.]
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Epidemiology (EPI)
DOI 10.1007/s00125-002-0829-2
Erfassungsdatum 2002-12-31
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