Erfordern neue biochemische Befunde ein Umdenken bei der Therapie des Typ-2-Diabetes?

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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