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Kantartzis, K.

Pathophysiologie der mitmetabolischer Dysfunktionassoziierten steatotischenLebererkrankung.

Pathophysiology of the metabolic dysfunction-associated steatotic liver disease.

Diabetologie 22, 221–231 (2026)
DOI
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Metabolic dysfunction-associated steatotic liver disease (MASLD) has long been considered the hepatic manifestation of the metabolic syndrome. Even today, an unhealthy lifestyle, especially overeating and lack of physical activity, and the resulting obesity and insulin resistance are considered the main causes of MASLD. However, new findings have shown that the steatotic and often inflamed liver (metabolic dysfunction-associated steatohepatitis [MASH]) plays an important role in the development of insulin resistance, hyperglycemia, and dyslipidemia, and thus also of cardiovascular events. MASH can progress to fibrosis, cirrhosis, and hepatocellular carcinoma. Recent data suggest that MASLD is a heterogeneous disease. For instance, “typical” MASLD, as described above, can also occur in normal weight or even underweight patients. In this case, the prevailing view is that there is “dysfunctional” white adipose tissue with reduced storage capacity and unfavorable adipokine secretion, especially low adiponectin production. Furthermore, there is a form of MASLD that is not accompanied by severe insulin resistance. This type of MASLD is usually characterized by mutations in the PNPLA3 and TM6SF2 genes. National and international guidelines for the treatment of MASLD primarily favor weight loss. Drugs that are currently approved for the treatment of MASH and fibrosis F2–F3, and those that are still under investigation, could in the future enable a pathophysiology-based and more efficient therapy for MASLD.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Leitlinie
Schlagwörter Hepatic Steatosis ; Insulin Resistance ; Mash ; Masld ; Metabolic Syndrome; Nonalcoholic Fatty Liver; Fetuin-a; Insulin-resistance; Risk; Consequences; Obesity; Adiposity; Genetics; Agonist; Variant
ISSN (print) / ISBN 2731-7447
e-ISSN 2731-7455
Zeitschrift Diabetologie, Die
Quellenangaben Band: 22, Heft: , Seiten: 221–231 Artikelnummer: , Supplement: ,
Verlag Springer
Verlagsort Tiergartenstrasse 17, D-69121 Heidelberg, Germany
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes Research and Metabolic Diseases (IDM)