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DOI: 10.1055/s-2006-956279
© Georg Thieme Verlag KG Stuttgart · New York
Rolle von Muskulatur und Fettgewebe in der Pathogenese des Typ-2-Diabetes
Role of muscle and fat in the pathogenesis of type 2 diabetesPublikationsverlauf
                     eingereicht: 1.3.2006
                     
                     akzeptiert: 6.7.2006
                     
Publikationsdatum:
30. November 2006 (online)

Zusammenfassung
In den letzten Jahren tritt der Diabetes mellitus Typ 2 nahezu epidemisch auf. Weltweit sind mehr als 170 Millionen Menschen betroffen, allein in Deutschland leben ˜ 6 Millionen Erkrankte. In der Pathogenese des Typ-2-Diabetes spielt die Kombination aus Insulinresistenz von Fettgewebe, Muskulatur und Leber mit einem zunehmenden Insulinsekretionsdefekt der pankreatischen β-Zelle eine zentrale Rolle. Dabei sind sowohl genetische Faktoren als auch Umwelteinflüsse entscheidend an der Entstehung eines Typ-2-Diabetes beteiligt, wobei die genauen pathogenetischen Mechanismen noch weitgehend unbekannt sind. Zur Beurteilung der Bedeutung von Muskulatur, Leber und Fettgewebe bei der Ausprägung des Typ-2-Diabetes hat die Generierung gewebespezifischer Insulinrezeptor-Knockout-Mausmodelle wesentlich zum Verständnis der Rolle dieser Organe der Insulinresistenz beigetragen.
Summary
In the last years type 2 diabetes has reached almost epidemic proportions. More than 170 million individuals are affected worldwide, about ˜ 6 million in Germany. In the pathogenesis of type 2 diabetes, insulin resistance in liver, fat and muscle as well as the inability of the pancreatic β-cell to fully compensate for this insulin resistance are the central pathophysiological events. Both genetic and environmental factors, such as lack of physical exercise and hypercaloric nutrition play a major role in this process, although the precise mechanisms for type 2 diabetes development remain largely unknown. In the characterization of the role of liver, adipose tissue and skeletal muscle in the pathogenesis of type 2 diabetes, tissue specific knockout mouse models have challenged our concepts of glucose homeostasis.
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Prof. Dr. med. Matthias Blüher
         Universität Leipzig, Medizinische Klinik und Poliklinik III
         
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