2.50
Hdl Handle:
http://hdl.handle.net/10033/332803
Title:
Fatty acid elongation in non-alcoholic steatohepatitis and hepatocellular carcinoma.
Authors:
Kessler, Sonja M; 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 K
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.
Citation:
Fatty acid elongation in non-alcoholic steatohepatitis and hepatocellular carcinoma. 2014, 15 (4):5762-73 Int J Mol Sci
Journal:
International journal of molecular sciences
Issue Date:
2014
URI:
http://hdl.handle.net/10033/332803
DOI:
10.3390/ijms15045762
PubMed ID:
24714086
Type:
Article
Language:
en
ISSN:
1422-0067
Appears in Collections:
publications of the department of microbial natural substances ([HIPS]MINS)

Full metadata record

DC FieldValue Language
dc.contributor.authorKessler, Sonja Men
dc.contributor.authorSimon, Yvetteen
dc.contributor.authorGemperlein, Katjaen
dc.contributor.authorGianmoena, Kathrinen
dc.contributor.authorCadenas, Cristinaen
dc.contributor.authorZimmer, Vincenten
dc.contributor.authorPokorny, Julianeen
dc.contributor.authorBarghash, Ahmaden
dc.contributor.authorHelms, Volkharden
dc.contributor.authorvan Rooijen, Nicoen
dc.contributor.authorBohle, Rainer Men
dc.contributor.authorLammert, Franken
dc.contributor.authorHengstler, Jan Gen
dc.contributor.authorMueller, Rolfen
dc.contributor.authorHaybaeck, Johannesen
dc.contributor.authorKiemer, Alexandra Ken
dc.date.accessioned2014-10-15T13:13:54Z-
dc.date.available2014-10-15T13:13:54Z-
dc.date.issued2014-
dc.identifier.citationFatty acid elongation in non-alcoholic steatohepatitis and hepatocellular carcinoma. 2014, 15 (4):5762-73 Int J Mol Scien
dc.identifier.issn1422-0067-
dc.identifier.pmid24714086-
dc.identifier.doi10.3390/ijms15045762-
dc.identifier.urihttp://hdl.handle.net/10033/332803-
dc.description.abstractNon-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.en
dc.language.isoenen
dc.rightsArchived with thanks to International journal of molecular sciencesen
dc.titleFatty acid elongation in non-alcoholic steatohepatitis and hepatocellular carcinoma.en
dc.typeArticleen
dc.identifier.journalInternational journal of molecular sciencesen

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