Zusammenfassung
Gesteigerte Insulinsekretion bei Patienten mit Insulinresistenz und Typ-2-Diabetes
führt zu endoplasmatischem Retikulum-Stress mit Störungen von Proteostase und Proteinfaltung.
Wenn die protektiven Stoffwechselwege der unfolded protein response den endoplasmatischen
Retikulum-Stress nicht reduzieren können, kommt es offenbar infolge gesteigerter Apoptose
zu Verlust von β-Zellen und einer Progression der diabetischen Krankheit. Therapeutische
Strategien sollten die Anforderungen an die β-Zelle beschränken. Die Restriktion langwirkender
Sulfonylharnstoffe und eine frühere Insulingabe werden diskutiert.
Abstract
Increased insulin secretion in patients with insulin resistance and type 2 diabetes
leads to endoplasmic reticulum stress with disturbances of proteostasis and protein
folding. If the protective pathways of the unfolded protein response fail to diminish
the ER stress, pancreatic β-cells loss by apoptosis appears to play an important role
in the progression of the disease. Therapeutic approaches should relieve the demand
on the β-cells by restriction of long-acting sulfonylureas but earlier administration
of insulin.
Schlüsselwörter
Typ-2-Diabetes - endoplasmatischer Retikulum-Stress - unfolded protein response -
Apoptose - Sulfonylharnstoffe - Insulin
Key words
type 2 diabetes - endoplasmic reticulum stress - unfolded protein response - apoptosis
- sulfonylureas - insulin
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Prof. Dr. med. W. Bruns
Smetanastr. 15
13088 Berlin
Telefon: 0 30 / 92 40 52 16
Fax: 0 30 / 92 40 52 16
eMail: waldemarbruns@web.de