Adipose-derived autotaxin regulates inflammation and steatosis associated with diet-induced obesity.


Journal

PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081

Informations de publication

Date de publication:
2019
Historique:
received: 12 06 2018
accepted: 12 11 2018
entrez: 8 2 2019
pubmed: 8 2 2019
medline: 30 10 2019
Statut: epublish

Résumé

Autotaxin (ATX) is a secreted enzyme that generates the bioactive lipid lysophosphatidic acid (LPA). We generated mice with global inducible post-natal inactivation or adipose-specific loss of the Enpp2 gene encoding ATX. The animals are phenotypically unremarkable and exhibit differences in adipocyte size and adipose tissue expression of inflammatory genes after high fat feeding without gross differences in fat distribution or body mass. Surprisingly, both models of Enpp2- deficiency exhibited marked protection from high fat diet-induced hepatic steatosis. This phenotype was not associated with differences in dietary fat absorption but may be accounted for by differences in hepatic expression of genes involved in de novo synthesis of triglycerides. These findings suggest that pharmacological inhibition of ATX might be protective against hepatic steatosis.

Identifiants

pubmed: 30730895
doi: 10.1371/journal.pone.0208099
pii: PONE-D-18-17633
pmc: PMC6366870
doi:

Substances chimiques

Dietary Fats 0
Lysophospholipids 0
Triglycerides 0
Phosphoric Diester Hydrolases EC 3.1.4.-
alkylglycerophosphoethanolamine phosphodiesterase EC 3.1.4.39
lysophosphatidic acid PG6M3969SG

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

e0208099

Subventions

Organisme : NIGMS NIH HHS
ID : P20 GM103527
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL120507
Pays : United States

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

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Auteurs

J Anthony Brandon (JA)

Division of Cardiovascular Medicine, The Gill Heart and Vascular Institute, University of Kentucky, Lexington, KY, United States of America.

Maria Kraemer (M)

Division of Cardiovascular Medicine, The Gill Heart and Vascular Institute, University of Kentucky, Lexington, KY, United States of America.

Julia Vandra (J)

Division of Cardiovascular Medicine, The Gill Heart and Vascular Institute, University of Kentucky, Lexington, KY, United States of America.

Suchismita Halder (S)

Division of Cardiovascular Medicine, The Gill Heart and Vascular Institute, University of Kentucky, Lexington, KY, United States of America.

Margo Ubele (M)

Division of Cardiovascular Medicine, The Gill Heart and Vascular Institute, University of Kentucky, Lexington, KY, United States of America.

Andrew J Morris (AJ)

Division of Cardiovascular Medicine, The Gill Heart and Vascular Institute, University of Kentucky, Lexington, KY, United States of America.
Department of Veterans Affairs Medical Center, Lexington, Kentucky, United States of America.

Susan S Smyth (SS)

Division of Cardiovascular Medicine, The Gill Heart and Vascular Institute, University of Kentucky, Lexington, KY, United States of America.
Department of Veterans Affairs Medical Center, Lexington, Kentucky, United States of America.

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Classifications MeSH