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Diabetologie und Stoffwechsel 2011; 6(3): 159-163
DOI: 10.1055/s-0031-1271465
Übersicht

© 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?H. Fiedler, W. Bruns
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Publication History

Publication Date:
21 June 2011 (online)

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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

Phone: 0 30 / 92 40 52 16

Fax: 0 30 / 92 40 52 16

Email: waldemarbruns@web.de

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