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Interleukin-l-Receptor Antagonist in Type 2 Diabetes Mellitus
Oleh:
Larsen, Claus M.
;
Faulenbach, Mirjam
;
Yaag, Allan
;
Aage, Y. Lund
;
Ehses, Jan A
;
Seifert, Burkhardt
;
Mandrup-Poulsen,Thomas
;
Donath, Marc Y
Jenis:
Article from Journal - ilmiah internasional
Dalam koleksi:
The New England Journal of Medicine (keterangan: ada di Proquest) vol. 356 no. 15 (Apr. 2007)
,
page 1517.
Ketersediaan
Perpustakaan FK
Nomor Panggil:
N08.K.2007.02
Non-tandon:
1 (dapat dipinjam: 0)
Tandon:
tidak ada
Lihat Detail Induk
Isi artikel
BACKGROUND The expression ofinterleukin-1-receptor antagonist is reduced in pancreatic islets of FI patients with type 2 diabetes mellitus, and high glucose concentrations induce the production ofinterleukin-1ß in human pancreatic beta cells, leading to impaired insulin secretion, decreased cell proliferation, and apoptosis. METHODS In this double-blind, parallel-group trial involving 70 patients with type 2 diabetes, si we randomly assigned 34 patients to receive 100 mg of anakinra (a recombinant human interleukin-1-receptor antagonist) subcutaneously once daily for 13 weeks and 36 patients to receive placebo. At baseline and at 13 weeks, all patients underwent an oral glucose-tolerance test, followed by an intravenous bolus of 0.3 g of glucose per kilogram of body weight, 0.5 mg of glucagon, and 5 g of arginine. In addition, 35 patients underwent a hyperinsulinemic-euglycemic clamp study. The primary end point was a change in the level of glycated hemoglobin, and secondary [ end points were changes in beta-cell function, insulin sensitivity, and inflammatory markers. RESULTS At 13 weeks, in the anakinra group, the glycated hemoglobin level was 0.46 percentage point lower than in the placebo group (P=0.03); C-peptide secretion was enhanced (P=0.05), and there were reductions in the ratio of pro insulin to insulin (P=0.005) and in levels ofinterleukin-6 (P
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