Islet Inflammation in Type 2 Diabetes : From metabolic stress to therapy  

Oleh:

Donath, Marc Y. ; Schumann, Desiree M. ; Faulenbach, Mirjam ; Ellingsgaard, Helga

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Diabetes Care vol. 31 no. Sup 02 (Feb. 2008), page s161-s164.
Topik: IL; interleukin; KATP channel; ATP-sensitive K+ channel

Ketersediaan

Perpustakaan FK Nomor Panggil: D05.K.2008.01 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

Lihat Detail Induk

Isi artikel

Decreases in both mass and secretory function of insulin-producing ß-cells contribute to the pathophysiology of type 2 diabetes. The histology of islets from patients with type 2 diabetes displays an inflammatory process characterized by the presence of cytokines, apoptotic cells, immune cell infiltration, amyloid deposits, and eventually fibrosis. This inflammatory process is probably the combined consequence of dyslipidemia, hyperglycemia, and increased circulating adipokines. Therefore, modulation of intra-islet inflammatory mediators, in particular interleukin-1ß, appears as a promising therapeutic approach.

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