Please use this identifier to cite or link to this item: doi:10.22028/D291-27435
Title: Fatty Acid Elongation in Non-Alcoholic Steatohepatitis and Hepatocellular Carcinoma
Author(s): Keßler, Sonja Maria
Simon, Yvette
Gemperlein, Katja
Gianmoena, Kathrin
Cadenas, Cristina
Zimmer, Vincent
Pokorny, Juliane
Barghash, Ahmad
Helms, Volkhard
van Rooijen, Nico
Bohle, Rainer M.
Lammert, Frank
Hengstler, Jan G.
Mueller, Rolf
Haybaeck, Johannes
Kiemer, Alexandra
Language: English
Title: International Journal of Molecular Sciences
Volume: 15
Issue: 4
Startpage: 5762
Endpage: 5773
Publisher/Platform: MDPI
Year of Publication: 2014
DDC notations: 000 Generalities
570 Life sciences, biology
610 Medicine and health
Publikation type: Journal Article
Abstract: Non-alcoholic steatohepatitis (NASH) represents a risk factor for the development of hepatocellular carcinoma (HCC) and is characterized by quantitative and qualitative changes in hepatic lipids. Since elongation of fatty acids from C16 to C18 has recently been reported to promote both hepatic lipid accumulation and inflammation we aimed to investigate whether a frequently used mouse NASH model reflects this clinically relevant feature and whether C16 to C18 elongation can be observed in HCC development. Feeding mice a methionine and choline deficient diet to model NASH not only increased total hepatic fatty acids and cholesterol, but also distinctly elevated the C18/C16 ratio, which was not changed in a model of simple steatosis (ob/ob mice). Depletion of Kupffer cells abrogated both quantitative and qualitative methionine-and-choline deficient (MCD)-induced alterations in hepatic lipids. Interestingly, mimicking inflammatory events in early hepatocarcinogenesis by diethylnitrosamine-induced carcinogenesis (48 h) increased hepatic lipids and the C18/C16 ratio. Analyses of human liver samples from patients with NASH or NASH-related HCC showed an elevated expression of the elongase ELOVL6, which is responsible for the elongation of C16 fatty acids. Taken together, our findings suggest a detrimental role of an altered fatty acid pattern in the progression of NASH-related liver disease.
DOI of the first publication: 10.3390/ijms15045762
Link to this record: urn:nbn:de:bsz:291--ds-274351
hdl:20.500.11880/28530
http://dx.doi.org/10.22028/D291-27435
ISSN: 1422-0067
Date of registration: 3-Jan-2020
Faculty: NT - Naturwissenschaftlich- Technische Fakultät
Department: NT - Pharmazie
Professorship: HW - Prof. Dr. Heinz Kußmaul
Collections:SciDok - Der Wissenschaftsserver der Universität des Saarlandes

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