| Online-Ressource |
Verfasst von: | Pathil-Warth, Anita [VerfasserIn]  |
| Liebisch, Gerhard [VerfasserIn]  |
| Okun, Jürgen G. [VerfasserIn]  |
| Chamulitrat, Walee [VerfasserIn]  |
| Schmitz, Gerd [VerfasserIn]  |
| Stremmel, Wolfgang [VerfasserIn]  |
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 |
Ursodeoxycholyl lysophosphatidylethanolamide modifies aberrant lipid profiles in NAFLD / Pathil-Warth, Anita [VerfasserIn]; 24 June 2015 (Online-Ressource)