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Nichtalkoholische Fettleber

Definition und Entstehung

Non-alcoholic fatty liver disease

Definition and development

  • Leitthema
  • Published:
Der Diabetologe Aims and scope

Zusammenfassung

Nichtalkoholische Fettlebererkrankungen (NAFLD) reichen von Steatose (NAFL) über Fibrose und Steatohepatitis (NASH) zur kryptogenen Zirrhose. Die Diagnose der NAFL ist bei einem Fettgehalt von >5% des Lebergewichts und Ausschluss anderer Lebererkrankungen (z. B. Alkohol) gegeben. Bei der Entstehung sind verschiedene Mechanismen beteiligt. Hepatische und systemische Insulinresistenz bewirken Lipolyse im Fettgewebe, Anstieg freier Fettsäuren (FFS) im Plasma und Lipidspeicherung in der Leber, die auch durch hyperkalorische fettreiche Diät mit hohem glykämischem Index gefördert wird. Adipozytokine aus dem Fettgewebe verbessern (Adiponektin) oder verschlechtern (Tumornekrosefaktor α: TNFα, Interleukine) die Insulinsensitivität und Fettspeicherung. FFS und Störungen des Adipozytokingleichgewichts stimulieren Entzündungsreaktionen und oxidativen Stress, die nicht nur die Progression der Steatose zu NASH, sondern auch die systemische Inflammation mit ihren Folgen wie erhöhtem kardiovaskulärem Risiko steuern.

Abtract

Non-alcoholic fatty liver diseases (NAFLD) range from steatosis (NAFL), fibrosis, and steatohepatitis (NASH) to cryptogenic cirrhosis. The diagnosis is made when the liver fat content exceeds 5% of the liver’s weight and other liver diseases (e.g. alcoholism) have been ruled out. Various mechanisms are involved in the pathogenesis of NAFLD. Hepatic and systemic insulin resistance cause increased lipolysis by adipose tissue, raise plasma free fatty acids (FFA), and stimulate lipid deposition in the liver, which is augmented by hypercaloric high-fat diet with high glycemic index. Adipocytokines from adipose tissue improve (adiponectin) or impair (tumour necrosis factor alpha, interleukines) insulin sensitivity and lipid deposition. FFA and imbalance of adipocytokines stimulate inflammatory pathways and oxidative stress, controlling not only the progression of steatosis to NASH but also systemic inflammation with its consequences such as increased cardiovascular risk.

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Authors and Affiliations

  1. Karl-Landsteiner Institut für Endokrinologie und Stoffwechsel, Wien, Österreich

    M. Kacerovsky &  M. Roden

  2. 1. Medizinische Abteilung, Hanusch-Krankenhaus, Heinrich-Collin-Straße 30, 1140, Wien, Österreich

    M. Roden

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  1. M. Kacerovsky
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  2. M. Roden
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Correspondence to M. Roden.

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Kacerovsky, M., Roden, M. Nichtalkoholische Fettleber. Diabetologe 3, 176–183 (2007). https://doi.org/10.1007/s11428-007-0130-6

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  • DOI: https://doi.org/10.1007/s11428-007-0130-6

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