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Verfasst von:Pathil-Warth, Anita [VerfasserIn]   i
 Liebisch, Gerhard [VerfasserIn]   i
 Okun, Jürgen G. [VerfasserIn]   i
 Chamulitrat, Walee [VerfasserIn]   i
 Schmitz, Gerd [VerfasserIn]   i
 Stremmel, Wolfgang [VerfasserIn]   i
Titel:Ursodeoxycholyl lysophosphatidylethanolamide modifies aberrant lipid profiles in NAFLD
Verf.angabe:Anita Pathil, Gerhard Liebisch, Jürgen G. Okun, Walee Chamulitrat, Gerd Schmitz and Wolfgang Stremmel
E-Jahr:2015
Jahr:24 June 2015
Umfang:7 S.
Fussnoten:Gesehen am 01.07.2020
Titel Quelle:Enthalten in: European journal of clinical investigation
Ort Quelle:Oxford [u.a.] : Wiley-Blackwell, 1970
Jahr Quelle:2015
Band/Heft Quelle:45(2015), 9, Seite 925-931
ISSN Quelle:1365-2362
Abstract:Background Hepatic fat accumulation with disturbed lipid homoeostasis is a hallmark of nonalcoholic fatty liver disease (NAFLD). The bile acid phospholipid conjugate Ursodeoxycholyl lysophosphatidylethanolamide (UDCA-LPE) is a novel anti-inflammatory agent with hepatoprotective effects in murine high-fat-diet (HFD)-induced NAFLD. The aim of this work was to study changes in the hepatic lipidome due to UDCA-LPE. Materials and methods High fat diet mouse model, mass spectometry, RT-PCR. Results Hepatic lipid extracts of HFD mice were analysed by mass spectrometry. The results determined higher levels of total, saturated, mono- and diunsaturated fatty acids (FA) in HFD mice, which were decreased by UDCA-LPE predominantly by the reducing the most abundant FA species palmitic acid and oleic acid. Unlike other FA species, levels of long-chain polyunsaturated fatty acids (LCPUFA), which are composed of arachidonic acid (ARA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), were increased in HFD mice upon UDCA-LPE treatment, mainly due to elevated hepatic ARA pools. Analysis of hepatic phospholipids species showed a decrease in total phosphatidylcholine (PC), especially monounsaturated PC (PUFA-PC) levels in HFD mice. Loss of total PC was reversed due to UDCA-LPE by increasing hepatic PUFA-PC pools. Gene expression analysis showed that UDCA-LPE upregulated PPARα, a key transcriptional regulator of fatty acid oxidation, as well as downstream target genes CPT1α and AOX, which are crucially involved in mitochondrial and peroxisomal fatty acid oxidation. Conclusion UDCA-LPE modulates defective fatty acid metabolism during experimental NAFLD thereby restoring altered lipid profiles in addition to its pronounced anti-inflammatory effects. Thus, UDCA-LPE may be a promising drug candidate for the management of NAFLD.
DOI:doi:10.1111/eci.12486
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext ; Verlag: https://doi.org/10.1111/eci.12486
 Volltext: https://onlinelibrary.wiley.com/doi/abs/10.1111/eci.12486
 DOI: https://doi.org/10.1111/eci.12486
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:Fatty acid composition
 non-alcoholic fatty liver disease
 UDCA-LPE
K10plus-PPN:1703013441
Verknüpfungen:→ Zeitschrift

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