Genetically modified mouse models to study hepatic neutral lipid mobilization.
Cholesterol
Fibrosis
Lipase
Liver
Neutral lipid metabolism
Non-alcoholic fatty liver disease
Retinol
Steatosis
Triacylglycerol
Vitamin A
Journal
Biochimica et biophysica acta. Molecular basis of disease
ISSN: 1879-260X
Titre abrégé: Biochim Biophys Acta Mol Basis Dis
Pays: Netherlands
ID NLM: 101731730
Informations de publication
Date de publication:
01 05 2019
01 05 2019
Historique:
received:
12
03
2018
revised:
25
05
2018
accepted:
01
06
2018
pubmed:
9
6
2018
medline:
28
11
2019
entrez:
9
6
2018
Statut:
ppublish
Résumé
Excessive accumulation of triacylglycerol is the common denominator of a wide range of clinical pathologies of liver diseases, termed non-alcoholic fatty liver disease. Such excessive triacylglycerol deposition in the liver is also referred to as hepatic steatosis. Although liver steatosis often resolves over time, it eventually progresses to steatohepatitis, liver fibrosis and cirrhosis, with associated complications, including liver failure, hepatocellular carcinoma and ultimately death of affected individuals. From the disease etiology it is obvious that a tight regulation between lipid uptake, triacylglycerol synthesis, hydrolysis, secretion and fatty acid oxidation is required to prevent triacylglycerol deposition in the liver. In addition to triacylglycerol, also a tight control of other neutral lipid ester classes, i.e. cholesteryl esters and retinyl esters, is crucial for the maintenance of a healthy liver. Excessive cholesteryl ester accumulation is a hallmark of cholesteryl ester storage disease or Wolman disease, which is associated with premature death. The loss of hepatic vitamin A stores (retinyl ester stores of hepatic stellate cells) is incidental to the onset of liver fibrosis. Importantly, this more advanced stage of liver disease usually does not resolve but progresses to life threatening stages, i.e. liver cirrhosis and cancer. Therefore, understanding the enzymes and pathways that mobilize hepatic neutral lipid esters is crucial for the development of strategies and therapies to ameliorate pathophysiological conditions associated with derangements of hepatic neutral lipid ester stores, including liver steatosis, steatohepatitis, and fibrosis. This review highlights the physiological roles of enzymes governing the mobilization of neutral lipid esters at different sites in liver cells, including cytosolic lipid droplets, endoplasmic reticulum, and lysosomes. This article is part of a Special Issue entitled Molecular Basis of Disease: Animal models in liver disease.
Identifiants
pubmed: 29883718
pii: S0925-4439(18)30205-9
doi: 10.1016/j.bbadis.2018.06.001
pmc: PMC6887554
mid: EMS85080
pii:
doi:
Substances chimiques
Lipase
EC 3.1.1.3
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
879-894Subventions
Organisme : Austrian Science Fund FWF
ID : I 3535
Pays : Austria
Informations de copyright
Copyright © 2018 Elsevier B.V. All rights reserved.
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