Group VIA phospholipase A2 deficiency in mice chronically fed with high-fat-diet attenuates hepatic steatosis by correcting a defect of phospholipid remodeling.


Journal

Biochimica et biophysica acta. Molecular and cell biology of lipids
ISSN: 1879-2618
Titre abrégé: Biochim Biophys Acta Mol Cell Biol Lipids
Pays: Netherlands
ID NLM: 101731727

Informations de publication

Date de publication:
05 2019
Historique:
received: 16 08 2018
revised: 22 01 2019
accepted: 25 01 2019
pubmed: 9 2 2019
medline: 4 12 2019
entrez: 9 2 2019
Statut: ppublish

Résumé

A defect of hepatic remodeling of phospholipids (PL) is seen in non-alcoholic fatty liver disease and steatohepatitis (NASH) indicating pivotal role of PL metabolism in this disease. The deletion of group VIA calcium-independent phospholipase A2 (iPla2β) protects ob/ob mice from hepatic steatosis (BBAlip 1861, 2016, 440-461), however its role in high-fat diet (HFD)-induced NASH is still elusive. Here, wild-type and iPla2β-null mice were subjected to chronic feeding with HFD for 6 months. We showed that protection was observed in iPla2β-null mice with an attenuation of diet-induced body and liver-weight gains, liver enzymes, serum free fatty acids as well as hepatic TG and steatosis scores. iPla2β deficiency under HFD attenuated the levels of 1-stearoyl lysophosphatidylcholine (LPC), lysophosphatidylethanolamine (LPE), and lysophosphatidylinositol (LPI) as well as elevation of hepatic arachidonate, arachidonate-containing cholesterol esters and prostaglandin E

Identifiants

pubmed: 30735855
pii: S1388-1981(18)30221-X
doi: 10.1016/j.bbalip.2019.01.012
pii:
doi:

Substances chimiques

Phospholipids 0
Group VI Phospholipases A2 EC 3.1.1.4
Pla2g6 protein, mouse EC 3.1.1.4

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

662-676

Informations de copyright

Copyright © 2019 Elsevier B.V. All rights reserved.

Auteurs

Ann-Christin Otto (AC)

Department of Internal Medicine IV, Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany.

Hongying Gan-Schreier (H)

Department of Internal Medicine IV, Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany.

Xingya Zhu (X)

Department of Internal Medicine IV, Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany.

Sabine Tuma-Kellner (S)

Department of Internal Medicine IV, Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany.

Simone Staffer (S)

Department of Internal Medicine IV, Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany.

Alexandra Ganzha (A)

Institute of Clinical Chemistry and Laboratory Medicine, University Regensburg, Franz-Josef-Strauss-Allee 11, 93053 Regensburg, Germany.

Gerhard Liebisch (G)

Institute of Clinical Chemistry and Laboratory Medicine, University Regensburg, Franz-Josef-Strauss-Allee 11, 93053 Regensburg, Germany.

Walee Chamulitrat (W)

Department of Internal Medicine IV, Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany. Electronic address: Walee.Chamulitrat@med.uni-heidelberg.de.

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Classifications MeSH