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Diabetologie und Stoffwechsel 2007; 2(4): 231-237
DOI: 10.1055/s-2007-981185
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© Georg Thieme Verlag Stuttgart · New York

Typ-2-Diabetes - Prävention und Progressionshemmung durch Glitazone

Type 2 Diabetes - Prevention and Inhibition of Progression by GlitazonesS. Matthaei1 , A. Pfützner2
  • 1Diabetes - Zentrum Quakenbrück, Fachabteilung für Diabetologie, Stoffwechselerkrankungen und Endokrinologie am Christlichen Krankenhaus
  • 2Institut für klinische Forschung und Entwicklung, Mainz
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Publication History

2007

2007

Publication Date:
05 July 2007 (online)

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Zusammenfassung

Die weltweit steigende Prävalenz des Typ-2-Diabetes und die daraus resultierende Zunahme von diabetischen Folgeerkrankungen stellen uns vor die Herausforderung, nachhaltige Therapiekonzepte zu entwickeln, um die individuellen Therapieziele zu erreichen und damit langfristig die immensen Kosten der Erkrankung (zzt. ∼ 25 Mrd. € / Jahr in Deutschland) zu reduzieren. Studien mit Typ-2-Diabetikern haben gezeigt, dass eine optimierte Blutzuckereinstellung und die konsequente Behandlung aller weiteren kardiovaskulären Risikofaktoren die Prognose der Patienten verbessern kann. Die zielwertorientierte und dauerhafte Kontrolle des Blutzuckerstoffwechsels, als ein zentrales Element der multifaktoriellen Therapie des Typ-2-Diabetes, ist nach wie vor häufig schwierig zu erreichen, da die β-Zelldysfunktion progredient ist und durch die herkömmlichen oralen Antidiabetika (z. B. Metformin, Sulfonylharnstoffe) nicht aufgehalten wird. Glitazone (Rosiglitazon und Pioglitazon) aus der Gruppe der Thiazolidindione, vermindern die Insulinresistenz und verbessern u. a. über eine Verminderung des Insulinbedarfs und der Abnahme der Gluko- und Lipotoxizität die Funktion der β-Zellen. Durch diesen ursächlichen Behandlungsansatz haben sie das Potenzial, die Progression der Erkrankung aufzuhalten. Vor diesem Hintergrund haben zwei große Outcome-Studien (DREAM und ADOPT) untersucht, ob sich durch den Einsatz von Rosiglitazon die Manifestation eines Typ-2-Diabetes bei Patienten mit gestörter Glukosetoleranz bzw. das Fortschreiten der Erkrankung im frühen Stadium des Typ-2-Diabetes verzögern oder verhindern lässt. Die Ergebnisse zeigen, dass Rosiglitazon sowohl im Rahmen der Prävention des Typ-2-Diabetes als auch nach Manifestation der Erkrankung günstige Effekte aufweist.

Abstract

The increasing prevalence of type 2 diabetes worldwide, associated with the respective increase in diabetic complications, demands for therapeutic concepts capable to reach treatment goals in an attempt to decrease the individual burden as well as the immense costs associated with the disease (in Germany currently ∼ 25 Bill. € / year) in the long run. Studies have shown, that optimized antihyperglycemic therapy as part of a multifactorial treatment approach including other cardiovascular risk factors, is effective to improve prognosis. Since β-cell dysfunction is progressive and can't be halted by conventional agents like metformin and sulfonylurea, the treat-to-target and durable control of glycaemia is still often difficult to achieve. Glitazones (rosiglitazone, pioglitazone) reduce insulin resistance and improve β-cell function primarily by decreasing gluco- and lipotoxicity via interacting with the nuclear transcription factor PPAR-γ. Due to this dual mode of action, combating the two major pathophysiological defects of type 2 diabetes, these substances have the potential to prevent the disease as well as to halt disease progression. Based on this background two large outcome-studies (DREAM and ADOPT) investigated the effect of rosiglitazone on the prevention to develop type 2 diabetes in an IGT / IFG population (DREAM) as well as on the inhibition of disease progression in newly diagnosed subjects with type 2 diabetes. The results of the studies suggest that treatment with rosiglitazone is effective in both preventing type 2 diabetes as well as in the treatment after manifestation of the disease.

Schlüsselwörter

Typ-2-Diabetes - Pathophysiologie - Glitazontherapie - ADOPT- und DREAM-Studie

Key words

type 2 diabetes - pathophysiology - Glitazone-therapy - ADOPT- and DREAM study

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Prof. Dr. med. S. Matthaei

Diabetes-Zentrum Quakenbrück · Fachabteilung für Diabetologie, Stoffwechselerkrankungen und Endokrinologie am Christlichen Krankenhaus

Danziger Str. 10

49610 Quakenbrück

Phone: 0 54 31/15 28 31

Fax: 0 54 31/15 28 33

Email: S.Matthaei@christliches-krankenhaus-ev.de

URL: http://www.diabeteszentrum-quakenbrueck.de

Prof. Dr. Dr. A. Pfützner

Geschäftsführer Forschung und Entwicklung · Institut für klinische Forschung und Entwicklung · IKFE GmbH

Parcusstr. 8

55116 Mainz

Phone: +49/61 31/5 76 36 10

Fax: 49/61 31/5 76 36 11

Email: AndreasP@ikfe.de

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