LPIAT1/MBOAT7 depletion increases triglyceride synthesis fueled by high phosphatidylinositol turnover.
fatty liver
hepatic fibrosis
lipid metabolism
lipids
Journal
Gut
ISSN: 1468-3288
Titre abrégé: Gut
Pays: England
ID NLM: 2985108R
Informations de publication
Date de publication:
01 2021
01 2021
Historique:
received:
09
01
2020
revised:
24
02
2020
accepted:
11
03
2020
pubmed:
8
4
2020
medline:
31
7
2021
entrez:
8
4
2020
Statut:
ppublish
Résumé
Non-alcoholic fatty liver disease (NAFLD) is a common prelude to cirrhosis and hepatocellular carcinoma. The genetic We generated the hepatocyte-specific The hepatocyte-specific We found a novel pathway fueling triglyceride synthesis in hepatocytes, by a direct metabolic flow of PI into triglycerides. Our findings provide an insight into the pathogenesis and therapeutics of NAFLD.
Identifiants
pubmed: 32253259
pii: gutjnl-2020-320646
doi: 10.1136/gutjnl-2020-320646
pmc: PMC7788230
doi:
Substances chimiques
Membrane Proteins
0
Phosphatidylinositols
0
Triglycerides
0
Acyltransferases
EC 2.3.-
MBOAT7 protein, human
EC 2.3.-
Mboat7 protein, mouse
EC 2.3.1-
lysophosphatidylinositol acyltransferase
EC 2.3.1.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
180-193Informations de copyright
© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY. Published by BMJ.
Déclaration de conflit d'intérêts
Competing interests: None declared.
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