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Leber und Diabetes

Leber als Opfer und Täter des metabolischen Syndroms

Liver and diabetes

Liver as victim and offender of the metabolic syndrome

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Zusammenfassung

Die nichtalkoholische Fettlebererkrankung („non-alcoholic fatty liver disease“, NAFLD) ist eine häufige Erkrankung, die 30 % der Bevölkerung und 70 % aller Typ-2-Diabetes-Patienten betrifft. Bei genetischer Prädisposition entsteht durch den Einfluss von Umweltfaktoren wie falsche Ernährung, Adipositas und mangelnde Bewegung eine Steatose der Leber. Auch wenn die Prognose der NAFLD eher gutartig ist, ist die Stoffwechselstörung als Motor der Insulinresistenz und der Diabetesentstehung zu sehen. Daneben ist die Lebersteatose auch ein Kofaktor für die Entstehung von makrovaskulären Folgekrankheiten. Für den klinischen Alltag ist die Unterscheidung einer NAFLD von der aggressiven nichtalkoholischen Steatohepatitis (NASH) wichtig, da diese zu Zirrhose und einem hepatozellulären Karzinom (HCC) führen kann. Im Vordergrund der Diagnostik stehen der Ausschluss anderer Lebererkrankungen und die Leberbiopsie. Letztere sollte zunehmend durch nichtinvasive Serumteste und Elastizitätsmessung der Leber ersetzt werden. Bislang stehen mit Lebensstilveränderung, Vitamin-E- und Pioglitazongabe nur wenige gesicherte Therapiemaßnahmen zur Verfügung. Hier ist aber in Kürze mit einer deutlichen Zunahme an therapeutischen Möglichkeiten zu rechnen.

Abstract

Non-alcoholic fatty liver disease (NAFLD) affects about 30 % of the general population and 70 % of patients with type 2 diabetes. The disease manifests as steatosis of the liver on the basis of a genetic predisposition through environmental factors, such as obesity, nutrition and lack of physical activity. Although NAFLD has a relatively benign prognosis, the hepatic metabolic disturbance causes insulin resistance and is strongly associated with the development of diabetes and cardiovascular diseases. It is important to distinguish NAFLD from non-alcoholic steatohepatitis (NASH) which can lead to cirrhosis and hepatocellular carcinoma (HCC). The diagnosis can be made by exclusion of other hepatic diseases and by liver biopsy. Future efforts will focus on substituting the need for a biopsy by the use of non-invasive serum markers and measurement of liver stiffness. Therapeutic options for patients with NASH are currently limited to lifestyle intervention and administration of pioglitazone and vitamin E; however, it is probable that further therapeutic options will be available in the future, some of which are currently being tested in clinical trials.

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Einhaltung ethischer Richtlinien

Interessenkonflikt. E. Jaeckel hat Vortrags- und Beraterhonorare der Firmen NovoNordisk, Eli Lilly, Sanofi Aventis und Astra Zeneca erhalten. Sämtliche Firmen sind Hersteller von GLP-1-Analoga. Diese Honorare stehen nicht im Zusammenhang mit der Therapie der NASH. R. Taubert und M.P. Manns geben an, dass kein Interessenkonflikt besteht. Der Beitrag enthält keine Studien an Menschen oder Tieren.

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Authors and Affiliations

  1. Klinik für Gastroenterologie, Hepatologie & Endokrinologie, Medizinische Hochschule Hannover, Carl Neuberg Str. 1, 30625, Hannover, Deutschland

    E. Jaeckel, R. Taubert & M.P. Manns

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  1. E. Jaeckel
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  2. R. Taubert
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  3. M.P. Manns
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Correspondence to E. Jaeckel.

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Jaeckel, E., Taubert, R. & Manns, M. Leber und Diabetes. Diabetologe 10, 405–417 (2014). https://doi.org/10.1007/s11428-014-1255-z

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