About: Apolipoprotein D Transgenic Mice Develop Hepatic Steatosis through Activation of PPARγ and Fatty Acid Uptake

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An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Apolipoprotein D Transgenic Mice Develop Hepatic Steatosis through Activation of PPARγ and Fatty Acid Uptake
Creator	Daneault, Caroline Labrie, Marilyne Lalonde, Simon Mounier, Catherine Najyb, Ouafa Rassart, Eric Thiery, Maxime Rosiers, Chrisitne
Source	PMC
abstract	Transgenic mice (Tg) overexpressing human apolipoprotein D (H-apoD) in the brain are resistant to neurodegeneration. Despite the use of a neuron-specific promoter to generate the Tg mice, they expressed significant levels of H-apoD in both plasma and liver and they slowly develop hepatic steatosis and insulin resistance. We show here that hepatic PPARγ expression in Tg mice is increased by 2-fold compared to wild type (WT) mice. Consequently, PPARγ target genes Plin2 and Cide A/C are overexpressed, leading to increased lipid droplets formation. Expression of the fatty acid transporter CD36, another PPARgamma target, is also increased in Tg mice associated with elevated fatty acid uptake as measured in primary hepatocytes. Elevated expression of AMPK in the liver of Tg leads to phosphorylation of acetyl CoA carboxylase, indicating a decreased activity of the enzyme. Fatty acid synthase expression is also induced but the hepatic lipogenesis measured in vivo is not significantly different between WT and Tg mice. In addition, expression of carnitine palmitoyl transferase 1, the rate-limiting enzyme of beta-oxidation, is slightly upregulated. Finally, we show that overexpressing H-apoD in HepG2 cells in presence of arachidonic acid (AA), the main apoD ligand, increases the transcriptional activity of PPARγ. Supporting the role of apoD in AA transport, we observed enrichment in hepatic AA and a decrease in plasmatic AA concentration. Taken together, our results demonstrate that the hepatic steatosis observed in apoD Tg mice is a consequence of increased PPARγ transcriptional activity by AA leading to increased fatty acid uptake by the liver.
has issue date	2015-06-17(xsd:dateTime)
bibo:doi	10.1371/journal.pone.0130230
bibo:pmid	26083030
has license	cc-by
sha1sum (hex)	6a3acbb2d3cf75b9cb9221b0d8acc32559ec4cf8
schema:url	https://doi.org/10.1371/journal.pone.0130230
resource representing a document's title	Apolipoprotein D Transgenic Mice Develop Hepatic Steatosis through Activation of PPARγ and Fatty Acid Uptake
has PubMed Central identifier	PMC4470830
has PubMed identifier	26083030
schema:publication	PLoS One
resource representing a document's body	covid:6a3acbb2d3cf75b9cb9221b0d8acc32559ec4cf8#body_text
is schema:about of	named entity 'vivo' named entity 'addition' named entity 'fatty acid' named entity 'cells' named entity 'upregulated' named entity 'hepatic' named entity 'concentration' named entity 'PPARγ' named entity 'FATTY ACID' named entity 'HEPATIC STEATOSIS' named entity 'HEPATIC STEATOSIS' named entity 'ROLE' named entity 'LIVER' named entity 'COMPARED' named entity 'NEURODEGENERATION' named entity 'PPARGAMMA' named entity 'RESISTANT TO' named entity 'SLIGHTLY' named entity 'ELEVATED' named entity 'INCREASED' named entity 'OUR' named entity 'FORMATION' named entity 'PPAR' named entity 'SLOWLY' named entity 'LIPID DROPLETS' named entity 'INDUCED' named entity 'ADDITION' named entity 'EXPRESSION' named entity 'DECREASED ACTIVITY' named entity 'APOLIPOPROTEIN D' named entity 'GENERATE' named entity 'UPREGULATED' named entity 'ACETYL COA CARBOXYLASE' named entity 'ENZYME' named entity 'PRESENCE OF' named entity 'IN VIVO' named entity 'DIFFERENT' named entity 'WILD TYPE' named entity 'FATTY ACID SYNTHASE' named entity 'GENES' named entity 'UPTAKE' named entity 'LEADING' named entity 'HEPATIC' named entity 'LEVELS' named entity 'RESULTS' named entity 'LIPOGENESIS' named entity 'SIGNIFICANT' named entity 'AMPK' named entity 'PPAR' named entity 'ACTIVATION' named entity 'PRIMARY HEPATOCYTES' named entity 'DECREASE' named entity 'ENRICHMENT' named entity 'INCREASES' named entity 'TRANSPORTER' named entity 'APOD' named entity 'BUT' named entity 'HERE' named entity 'LEADS' named entity 'UPTAKE' named entity 'RATE-LIMITING' named entity 'TRANSGENIC MICE' named entity 'APOLIPOPROTEIN D' named entity 'FOLD' named entity 'ARACHIDONIC ACID' named entity '28H' named entity 'INDICATING' named entity 'TAKEN' named entity 'THE BRAIN' named entity 'PALMITOYL' named entity 'INSULIN RESISTANCE' named entity 'HEPG2' named entity 'FATTY ACID' named entity 'PLASMA'

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