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DOI: 10.1055/s-0031-1271465
© Georg Thieme Verlag KG Stuttgart ˙ New York
Erfordern neue biochemische Befunde ein Umdenken bei der Therapie des Typ-2-Diabetes?
Stimulierung oder Schonung der β-Zellen?Do New Biochemical Data Require a Change in the View of the Therapy of Type 2 Diabetes?Stimulation or Protection of the β-Cells?Publication History
Publication Date:
21 June 2011 (online)
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
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