117-81-7BJQHLKABXJIVAM-UHFFFAOYNA-NBJQHLKABXJIVAM-UHFFFAOYSA-N
Di(2-ethylhexyl) phthalate1,2-Benzenedicarboxylic acid, bis(2-ethylhexyl) ester
DEHP
1,2-Benzedicarboxylic acid, bis(2-ethyl-hexyl) ester
1,2-Benzenedicarboxylic acid bis(2-ethylhexyl) ester
1,2-Benzenedicarboxylic acid, 1,2-bis(2-ethylhexyl) ester
1,2-Benzenedicarboxylic acid,bis(2-ethylhexylester)
Bis(2-ethylhexyl) 1,2-benzenedicarboxylate
Bis(2-ethylhexyl) o-phthalate
bis(2-ethylhexyl) phthalate
Bis(2-ethylhexyl)phthalat
Bis(2-ethylhexyl)phthalate
Bisoflex 81
Bisoflex DOP
Corflex 400
Di(2-ethylhexyl)phthalate
Di(isooctyl) phthalate
Di-2-ethylhexlphthalate
Di-2-ethylhexyl phthalate
DI-2-ETHYLHEXYL-PHTHALATE
Diacizer DOP
Diethylhexyl phthalate
Dioctylphthalate
DOF
Ergoplast FDO
Ergoplast FDO-S
ETHYLHEXYL PHTHALATE
Eviplast 80
Eviplast 81
Fleximel
Flexol DOD
Flexol DOP
ftlalato de bis(2-etilhexilo)
Garbeflex DOP-D 40
Good-rite GP 264
Hatco DOP
Jayflex DOP
Kodaflex DEHP
Kodaflex DOP
Monocizer DOP
NSC 17069
Palatinol AH
Palatinol AH-L
Phtalate de Bis (Ethyle-2-Hexyle)
Phtalate de bis(2-ethylhexyle)
PHTHALATE, BIS(2-ETHYLHEXYL)
Phthalic acid di(2-ethylhexyl) ester
Phthalic acid, bis(2-ethylhexyl) ester
PHTHALIC ACID, BIS(2-ETHYLHEXYL)ESTER
PHTHALSAEURE-BIS-(2-AETHYLHEXYL)-ESTER
Pittsburgh PX 138
Plasthall DOP
Reomol D 79P
Sansocizer DOP
Sansocizer R 8000
Sconamoll DOP
Staflex DOP
Truflex DOP
Vestinol AH
Vinycizer 80
Vinycizer 80K
Witcizer 312
DTXSID5020607637-07-0KNHUKKLJHYUCFP-UHFFFAOYSA-NKNHUKKLJHYUCFP-UHFFFAOYSA-N
Clofibrateethyl-p-chlorophenoxyisobutyrate
Propanoic acid, 2-(4-chlorophenoxy)-2-methyl-, ethyl ester
2-(p-Chlorophenoxy)-2-methylpropionic acid ethyl ester
Abitrate
Amotril
Anparton
Arteriosan
Artevil
Ateculon
Ateriosan
Atheropront
Atromid S
Atromidin
Azionyl
Bioscleran
Cartagyl
Claripex
Claripex CPIB
Clobren SF
Clofibrat
clofibrato
Clofinit
Ethyl (p-chlorophenoxy) isobutyrate
Ethyl 2-(4-chlorophenoxy)-2-methylpropionate
Ethyl 2-(4-chlorophenoxy)isobutyrate
Ethyl 2-(p-chlorophenoxy)-2-methylpropionate
Ethyl 2-(p-chlorophenoxy)isobutyrate
Ethyl clofibrate
Ethyl p-chlorophenoxyisobutyrate
Ethyl α-(4-chlorophenoxy)isobutyrate
Ethyl α-(4-chlorophenoxy)-α-methylpropionate
Ethyl α-(p-chlorophenoxy)isobutyrate
Ethyl α-(p-chlorophenoxy)-α-methylpropionate
Hyclorate
Lipavil
Lipavlon
Lipomid
Liprinal
Miscleron
Misclerone
Neo-Atromid
Normolipol
NSC 79389
p-Chlorophenoxyisobutyric acid ethyl ester
Propionic acid, 2-(p-chlorophenoxy)-2-methyl-, ethyl ester
Recolip
Regelan
Serotinex
Sklerepmexe
Sklerolip
Skleromexe
Sklero-Tablinene
Ticlobran
Xyduril
DTXSID30203363771-19-5XJGBDJOMWKAZJS-UHFFFAOYNA-NXJGBDJOMWKAZJS-UHFFFAOYSA-N
NafenopinDTXSID802091152214-84-3KPSRODZRAIWAKH-UHFFFAOYNA-NKPSRODZRAIWAKH-UHFFFAOYSA-N
CiprofibrateDTXSID802033125812-30-0HEMJJKBWTPKOJG-UHFFFAOYSA-NHEMJJKBWTPKOJG-UHFFFAOYSA-N
GemfibrozilPentanoic acid, 5-(2,5-dimethylphenoxy)-2,2-dimethyl-
2,2-Dimethyl-5-(2,5-xylyloxy)valeric acid
5-(2,5-Dimethylphenoxy)-2,2-dimethylpentanoic acid
Decrelip
gemfibrozilo
Gevilon
Lopizid
Trialmin 900
Valeric acid, 2,2-dimethyl-5-(2,5-xylyloxy)-
DTXSID002065241859-67-0IIBYAHWJQTYFKB-UHFFFAOYSA-NIIBYAHWJQTYFKB-UHFFFAOYSA-N
BezafibratePropanoic acid, 2-[4-[2-[(4-chlorobenzoyl)amino]ethyl]phenoxy]-2-methyl-
Befizal
Benzofibrate
Bezafibrat
bezafibrato
Bezalip
Bezatol
Difaterol
DTXSID302986949562-28-9YMTINGFKWWXKFG-UHFFFAOYSA-NYMTINGFKWWXKFG-UHFFFAOYSA-N
FenofibratePropanoic acid, 2-[4-(4-chlorobenzoyl)phenoxy]-2-methyl-, 1-methylethyl ester
2-[4-(4-Chlorobenzoyl)phenoxy]-2-methylpropanoic acid 1-methylethyl ester
Ankebin
Clorofibrate
Elasterin
Fenobrate
Fenofibrat
fenofibrato
Fenogal
Fenotard
Isopropyl 2-[p-(p-chlorobenzoyl)phenoxy]-2-methylpropionate
Lipanthyl
Lipantil
Lipicard
Lipidil
Lipidil Supra
Lipirex
Lipoclar
Lipofene
Liposit
MeltDose
Nolipax
NSC 281319
Procetofen
Procetofene
Procetoken
Protolipan
Secalip
DTXSID202987479902-63-9RYMZZMVNJRMUDD-HGQWONQESA-NRYMZZMVNJRMUDD-HGQWONQESA-N
SimvastatinButanoic acid, 2,2-dimethyl-, (1S,3R,7S,8S,8aR)-1,2,3,7,8,8a-hexahydro-3,7-dimethyl-8-[2-[(2R,4R)-tetrahydro-4-hydroxy-6-oxo-2H-pyran-2-yl]ethyl]-1-naphthalenyl ester
(+)-Simvastatin
Apo-Simvastatin
Bestatin 20
Butanoic acid, 2,2-dimethyl-, 1,2,3,7,8,8a-hexahydro-3,7-dimethyl-8-[2-(tetrahydro-4-hydroxy-6-oxo-2H-pyran-2-yl)ethyl]-1-naphthalenyl ester, [1S-[1α,3α,7β,8β(2S*,4S*),8aβ]]-
Cholestat
Co-Simvastatin
Kolestevan
L 644128-000U
Lipinorm
Liponorm
Lipovas
Lodales
Modutrol
Nor-Vastina
Novo-Simvastatin
Pms-simvastatin
Simastin 20
Simovil
Simvastatin lactone
Simvotin
Sinvacor
Sinvascor
Sivastin
Starstat 20
Synvinolin
Valemia
Velostatin
DTXSID0023581PR:000011170nuclear factor erythroid 2-related factor 2PR:000011396bile acid receptorPR:000011391nuclear receptor subfamily 0 group B member 2PR:000013056peroxisome proliferator-activated receptor alphaPR:00000877817-beta-hydroxysteroid dehydrogenase 14CHEBI:35366fatty acidPR:000011395oxysterols receptor LXR-alphaPR:000015611sterol regulatory element-binding protein 1PR:000003392microsomal triglyceride transfer protein large subunit MTTPPR:000004145apolipoprotein B-100CHEBI:17855triglycerideGO:0023052signalingGO:0035357peroxisome proliferator activated receptor signaling pathwayGO:0003824catalytic activityGO:0006635fatty acid beta-oxidationHP:0001397Hepatic steatosisGO:0032933SREBP signaling pathwayGO:0010467gene expressionGO:0009058biosynthetic processGO:0006633fatty acid biosynthetic process1increased2decreasedDi(2-ethylhexyl) phthalate2016-11-29T18:42:262016-11-29T18:42:26Mono(2-ethylhexyl) phthalate2016-11-29T18:42:262016-11-29T18:42:26Stressor:205 pirinixic acid (WY-14,643)2020-12-19T09:06:202020-12-19T09:06:20Clofibrate2016-11-29T18:42:272016-11-29T18:42:27Nafenopin2016-11-29T18:42:272016-11-29T18:42:27ciprofibrate2016-11-29T18:42:272016-11-29T18:42:27Gemfibrozil<p>Fibrate drug</p>
2016-11-29T18:42:272020-03-31T10:24:40PERFLUOROOCTANOIC ACID2016-11-29T18:42:272016-11-29T18:42:27Bezafibrate2016-11-29T18:42:272016-11-29T18:42:27Fenofibrate2016-11-29T18:42:272016-11-29T18:42:27Simvastatin2020-05-06T09:41:352020-05-06T09:41:3510116rat10090mouseWCS_9606humanWikiUser_28VertebratesActivation, NRF2Activation, NRF2MolecularCL:0000182hepatocyte2016-11-29T18:41:252017-09-16T10:15:20Activation, NR1H4Activation, NR1H4MolecularCL:0000182hepatocyte2016-11-29T18:41:252017-09-16T10:15:20Activation, SHPActivation, SHPMolecularCL:0000182hepatocyte2016-11-29T18:41:252017-09-16T10:15:20Activation, PPARαActivation, PPARαMolecular<p>Gene expression occurs in a coordinated fashion (Judson et al., 2012). The many observations of altered gene expression following binding of ligand to PPARα led to systematic investigations of the genomic signature that corresponds to PPARα activation (Tamura et al., 2006; Kupershmidt et al., 2010; Rosen et al., 2017; Rooney et al., 2018; Corton et al., 2020; Hill et al., 2020; Lewis et al., 2020). Specific gene with increased expression following PPARα activation include Cyp4a1, Cpt1B, and Lpl. More generally, the pathways activated include:</p>
<ul>
<li>Genes involved in Metabolism of lipids and lipoproteins</li>
<li>Fatty acid metabolism</li>
<li>Genes involved in Fatty acid, triacylglycerol, and ketone body metabolism</li>
<li>PPAR signaling pathway</li>
<li>Peroxisome</li>
<li>Genes involved in Cell Cycle</li>
</ul>
<p><strong>Biological state</strong></p>
<p>The Peroxisome Proliferator Activated receptor α (PPARα) belongs to the <a href="/wiki/index.php/Peroxisome_Proliferator_Activated_receptors_(PPARs;_NR1C)" title="Peroxisome Proliferator Activated receptors (PPARs; NR1C)">Peroxisome Proliferator Activated receptors (PPARs; NR1C)</a> steroid/thyroid/retinoid receptor superfamily of transcription factors.</p>
<p><strong>Biological compartments</strong></p>
<p>PPARα is expressed in high levels in tissues that perform significant catabolism of fatty acids (FAs), such as brown adipose tissue, liver, heart, kidney, and intestine (Michalik et al. 2006). The receptor is present also in skeletal muscle, intestine, pancreas, lung, placenta and testes (Mukherjee et al. 1997), (Schultz et al. 1999).</p>
<p><strong>General role in biology</strong></p>
<p>PPARs are activated by fatty acids and their derivatives; they are sensors of dietary lipids and are involved in lipid and carbohydrate metabolism, immune response and peroxisome proliferation (Wahli and Desvergne 1999), (Evans, Barish, & Wang, 2004). PAPRα is a also a target of hypothalamic hormone signalling and was found to play a role in embryonic development (Yessoufou and Wahli 2010).</p>
<p>Fibrates, activators of PPARα, are commonly used to treat hypertriglyceridemia and other dyslipidemic states as they have been shown to decrease circulating lipid levels (Lefebvre et al. 2006).</p>
<p>Binding of ligands to PPARα is measured using binding assays in vitro and in silico, whereas the information about functional activation is derived from transactivation assays (e.g. transactivation assay with reporter gene) that demonstrate functional activation of a nuclear receptor by a specific compound. Binding of agonists within the ligand-binding site of PPARs causes a conformational change of nuclear receptor that promotes binding to transcriptional co-activators. Conversely, binding of antagonists results in a conformation that favours the binding of co-repressors (Yu and Reddy 2007), (Viswakarma et al. 2010). Transactivation assays are performed using transient or stably transfected cells with the PPARα expression plasmid and a reporter plasmid, respectively. There are also other methods that have been used to measure PPARα activity, such as the Electrophoretic Mobility Shift Assay (EMSA) or commercially available PPARα transcription factor assay kits, see Table 1. The transactivation (stable transfection) assay provides the most applicable OECD Level 2 assay (i.e. In vitro assays providing mechanistic data) aimed at identifying the initiating event leading to an adverse outcome (LeBlanc, Norris, and Kloas 2011). A recent study characterized the PPARα ligand binding domain for the purpose of next-generation metabolic disease drugs (Kamata et al. 2020).</p>
<p>The most direct measure of this MIE is microarray profiling from<span style="font-size:medium"><span style="font-family:Cambria,serif"><span style="color:#000000"><span style="font-family:Calibri,sans-serif"><span style="color:#191c1f"> large gene expression databases TG-GATEs and DrugMatrix coupled with t statistical analysis of whole genome expression profiles (Svoboda et al., 2019; Igarashi et al., 2015) From these data, A gene expression signature of 131 PPARα-dependent genes was built using microarray profiles from the livers of wild-type and PPARα-null mice. A quantitative measure of this expression signature is a measure of similarity/correlation between the PPARα signature and positive and negative test sets is provided by the Running Fisher test (Corton et al., 2020; Hill et al., 2020; Kupershmidt et al., 2010; Lewis et al., 2020; Rooney et al., 2018).</span></span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:"Times New Roman",serif"><span style="color:#000000"><span style="font-family:Arial,sans-serif">A gene expression signature of 131 PPARα-dependent genes was built using microarray profiles from the livers of wild-type and PPARα-null mice. A quantitative measure of this expression signature would be a measure of similarity/correlation between the PPARα signature and positive and negative test sets is provided by the Running Fisher test </span><span style="font-family:Arial,sans-serif">(Kupershmidt et al., 2010; Rooney et al., 2018; Corton et al., 2020)</span><span style="font-size:10pt"><span style="font-family:Times">.</span></span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:"Times New Roman",serif"><span style="color:#000000"><span style="font-family:Arial,sans-serif">For all substances, MIE activation does not rise monotonically over dose or time. These fluctuations are likely due to variations in cofactor availability or access to the site of transcription </span><span style="font-family:Arial,sans-serif">(Gaillard et al., 2006; Koppen et al., 2009; Kupershmidt et al., 2010; Ong et al., 2010; Chow et al., 2011; De Vos et al., 2011; Simon et al., 2015)</span><span style="font-family:Arial,sans-serif">.</span></span></span></span></p>
<p><span style="font-size:12pt"><span style="color:#000000"><span style="font-family:Arial,sans-serif">. </span></span></span></p>
<table align="left" border="1" cellpadding="1" cellspacing="1" style="height:3px; width:100px">
<caption>Measurements of PPARα Activation</caption>
<thead>
<tr>
<th scope="row">Method/Test</th>
<th scope="col">Test Principle</th>
<th scope="col">Test Environment</th>
<th scope="col">Test Outcome</th>
<th scope="col">Assay Type/Domain</th>
</tr>
</thead>
<tbody>
<tr>
<th scope="row">
<p>molecular modelling; docking simulation</p>
</th>
<td>Computational simulation of ligand binding </td>
<td>In silico</td>
<td>Prediction off binding interaction </td>
<td>Quantitative virtual screeings</td>
</tr>
<tr>
<th scope="row">Scintillation proximity binding assay</th>
<td>Direct binding of ligand</td>
<td>In vitro</td>
<td>Identifies compouds that bind to PPARα</td>
<td>Qualitative in vitro screening</td>
</tr>
<tr>
<th scope="row">PPARα reporter gene assay</th>
<td>Quantify changes in in PPARα activation via a sensitive surrogate </td>
<td>In vitro, Ex vivo</td>
<td>Measures changes in activity of genes linked to a PPARα receptor element</td>
<td>Quantitative in vitro screening</td>
</tr>
<tr>
<th scope="row">Electrophoretic Band Shift</th>
<td>determines if a protein or protein mixture will bind to a specific DNA or RNA sequence</td>
<td>In vitro</td>
<td>Measures cofactor binding by changes in gel mobility</td>
<td>Quantitative in vitro screening</td>
</tr>
<tr>
<th scope="row">Microarray profiling</th>
<td>Develop MIE-specific sets of gene expression biomarkers</td>
<td>In vivo</td>
<td>Classification of PPARα biomarker genes with statistical methods</td>
<td>Quantitative in vivo screening</td>
</tr>
</tbody>
</table>
<p>PPARα has been identified in frog (Xenopus laevis), mouse, human, rat, fish, hamster and chicken (reviewed in (Wahli and Desvergne 1999)).</p>
UBERON:0002107liverCL:0000255eukaryotic cellHighHighHigh<p>Bhattacharya, Nandini, Jannette M Dufour, My-Nuong Vo, Janice Okita, Richard Okita, and Kwan Hee Kim. 2005. “Differential Effects of Phthalates on the Testis and the Liver.” Biology of Reproduction 72 (3) (March): 745–54. doi:10.1095/biolreprod.104.031583.</p>
<p>Bility, Moses T, Jerry T Thompson, Richard H McKee, Raymond M David, John H Butala, John P Vanden Heuvel, and Jeffrey M Peters. 2004. “Activation of Mouse and Human Peroxisome Proliferator-Activated Receptors (PPARs) by Phthalate Monoesters.” Toxicological Sciences : An Official Journal of the Society of Toxicology 82 (1) (November): 170–82. doi:10.1093/toxsci/kfh253.</p>
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<p>Corton, J. C., Hill, T., Sutherland, J. J., Stevens, J. L., & Rooney, J. (2020). A Set of Six Gene Expression Biomarkers Identify Rat Liver Tumorigens in Short-Term Assays. Toxicol Sci. https://doi.org/10.1093/toxsci/kfaa101</p>
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<p>Svoboda, D. L., Saddler, T., & Auerbach, S. S. (2019). An Overview of National Toxicology Program’s Toxicogenomic Applications: DrugMatrix and ToxFX. In Advances in Computational Toxicology (pp. 141-157). Springer. https://link.springer.com/chapter/10.1007/978-3-030-16443-0_8</p>
<p>ToxCastTM Data. “ToxCastTM Data.” US Environmental Protection Agency. <a class="external free" href="http://www.epa.gov/ncct/toxcast/data.html" rel="nofollow" target="_blank">http://www.epa.gov/ncct/toxcast/data.html</a></p>
<p>Vanden Heuvel, John P, Jerry T Thompson, Steven R Frame, and Peter J Gillies. 2006. “Differential Activation of Nuclear Receptors by Perfluorinated Fatty Acid Analogs and Natural Fatty Acids: A Comparison of Human, Mouse, and Rat Peroxisome Proliferator-Activated Receptor-Alpha, -Beta, and -Gamma, Liver X Receptor-Beta, and Retinoid X Rec.” Toxicological Sciences : An Official Journal of the Society of Toxicology 92 (2) (August): 476–89. doi:10.1093/toxsci/kfl014.</p>
<p>Venkata, Nagaraj Gopisetty, Jodie a Robinson, Peter J Cabot, Barbara Davis, Greg R Monteith, and Sarah J Roberts-Thomson. 2006. “Mono(2-Ethylhexyl)phthalate and Mono-N-Butyl Phthalate Activation of Peroxisome Proliferator Activated-Receptors Alpha and Gamma in Breast.” Toxicology Letters 163 (3) (June 1): 224–34. doi:10.1016/j.toxlet.2005.11.001.</p>
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2016-11-29T18:41:232020-12-28T12:48:16Decreased, DHB4/HSD17B4Decreased, DHB4/HSD17B4MolecularCL:0000182hepatocyte2016-11-29T18:41:252017-09-16T10:15:21Inhibition, Mitochondrial fatty acid beta-oxidationInhibition, Mitochondrial fatty acid beta-oxidationMolecularCL:0000182hepatocyte2016-11-29T18:41:242017-09-16T10:15:13Activation, LXR alphaActivation, LXR alphaMolecularCL:0000182hepatocyte2016-11-29T18:41:252017-09-16T10:15:21Increased, Liver SteatosisIncreased, Liver SteatosisOrgan<p>Biological state: liver steatosis is the inappropriate storage of fat in hepatocytes. <em>Four major pathways for triglyceride accumulation are: 1. Increased fatty acid uptake; 2. Increased De Novo FA and Lipid Synthesis; 3. Decreased FA Oxidation; 4. Decreased Lipid Efflux (Angrish et al. 2016). Chemical stressors can increase gene expression of key genes involving these pathways, leading to increased accumulation of triglycerides (Aguayo-Orozco et al. 2018). In addition, excessive dietary compounds of fatty compounds can also increase likelihood of accumulation of triglycerides (Nguyen et al. 2008). </em></p>
<p>Biological compartment: steatosis is generally an organ-level diagnosis; however, the pathology occurs within the hepatocytes.</p>
<p>Role in biology: steatosis is an adverse endpoint. </p>
<p> </p>
<p>Description from EU-ToxRisk:</p>
<p>Activation of stellate cells results in collagen accumulation and change in extracellular matrix composition in the liver causing fibrosis. (Landesmann, 2016)(Koo et al 2016)</p>
<p>Steatosis is measured by lipidomics approaches<em> (Yang and Han 2016)</em> that measure lipid levels, or by histology. <em>Concentrations of triglycerides, cholesterols, fatty acids, and related compounds are measured biochemically include high throughput enzymatic analyses, analytical ultracentrifuging, gradient gel electrophoresis, Nuclear Magnetic Resonance, and other direct assessment techniques (Schaefer et al. 2016).</em></p>
<p>Steatosis is the result of perturbations in well-known metabolic pathways that are well-studied and well-known in many taxa.</p>
<p><em>Life Stage: The life stage applicable to this key event is all life stages with a liver. Older individuals are more likely to manifest this adverse outcome pathway (adults > juveniles) due to accumulation of triglycerides.</em></p>
<p><em>Sex: This key event applies to both males and females.</em></p>
<p><em>Taxonomic: This key event appears to be present broadly in vertebrates, with most representative studies in mammals (humans, lab mice, lab rats).</em></p>
UBERON:0002107liverHighUnspecificHighAll life stagesHigh<p><em>Aguayo-Orozco, A.A., Bois, F.Y., Brunak, S., and Taboureau, O. 2018. Analysis of Time-Series Gene Expression Data to Explore Mechanisms of Chemical-Induced Hepatic Steatosis Toxicity. Frontiers in Genetics 9(Article 396): 1-15.</em></p>
<p><em>Angrish, M.M., Kaiser, J.P., McQueen, C.A., and Chorley, B.N. 2016. Tipping the Balance: Hepatotoxicity and the 4 Apical Key Events of Hepatic Steatosis. Toxicological Sciences 150(2): 261–268.</em></p>
<p>Landesmann, B. (2016). Adverse Outcome Pathway on Protein Alkylation Leading to Liver Fibrosis, (2).</p>
<p>https://doi.org/10.1016/j.molcel.2005.08.010</p>
<p>Koo, J. H., Lee, H. J., Kim, W., & Kim, S. G. (2016). Endoplasmic Reticulum Stress in Hepatic Stellate Cells Promotes Liver Fibrosis via PERK-Mediated Degradation of HNRNPA1 and Up-regulation of SMAD2. <em>Gastroenterology</em>, <em>150</em>(1), 181–193.e8. https://doi.org/10.1053/j.gastro.2015.09.039</p>
<p><em>Nguyen, P., Leray, V., Diez, M., Serisier, S., Le Bloc’h, J., Siliart, B., and Dumon, H. 2008. Liver lipid metabolism. Journal of Animal Physiology and Animal Nutrition 92: 272–283. </em></p>
<p><em>Schaefer EJ, Tsunoda F, Diffenderfer M, Polisecki, E., Thai, N., and Astalos, B. The Measurement of Lipids, Lipoproteins, Apolipoproteins, Fatty Acids, and Sterols, and Next Generation Sequencing for the Diagnosis and Treatment of Lipid Disorders. [Updated 2016 Mar 29]. In: Feingold KR, Anawalt B, Blackman MR, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK355892/</em></p>
<p><em>Yang, K. and Han, X. 2016. Lipidomics: Techniques, applications, and outcomes related to biomedical sciences. Trends in Biochemical Sciences 2016 November ; 41(11): 954–969.</em></p>
<p><em>NOTE: Italics symbolize edits from John Frisch</em></p>
2016-11-29T18:41:242024-03-26T13:17:41Inhibition, SREBP1cInhibition, SREBP1cMolecularCL:0000182hepatocyte2016-11-29T18:41:272017-09-16T10:15:21Activation, MTTPActivation, MTTPCellularCL:0000182hepatocyte2016-11-29T18:41:272017-09-16T10:15:22Increased, ApoB100Increased, ApoB100TissueUBERON:0000178blood2016-11-29T18:41:272017-09-16T10:15:22Increased, TriglycerideIncreased, TriglycerideCellularCL:0000182hepatocyte2016-11-29T18:41:272017-09-16T10:15:22Increased, De Novo FA synthesisIncreased, De Novo FA synthesisCellularCL:0000182hepatocyte2016-11-29T18:41:242017-09-16T10:15:16de2f11c4-c90d-4615-9e89-11ff04c205eaef588cdc-8d12-4463-b6cb-41ce63f9bc012016-11-29T18:41:342016-12-03T16:37:57ef588cdc-8d12-4463-b6cb-41ce63f9bc01398b12b4-3eb1-4e91-a096-965dc92a33f22016-11-29T18:41:342016-12-03T16:37:57ef588cdc-8d12-4463-b6cb-41ce63f9bc01ed0d4f0a-10a7-4f1c-ab49-7ecb974103dd2016-11-29T18:41:342016-12-03T16:37:58ed0d4f0a-10a7-4f1c-ab49-7ecb974103dd2772b496-48f7-4b4e-913a-92e583fc421c2016-11-29T18:41:342016-12-03T16:37:58a1961ff6-d06e-4674-a16c-8694c9619d484b4d51ad-8a40-45ec-a162-2ef6061c68c92016-11-29T18:41:342016-12-03T16:37:584b4d51ad-8a40-45ec-a162-2ef6061c68c9fc7e34d2-3b67-4709-a1fc-270ab32b64882016-11-29T18:41:342016-12-03T16:37:58398b12b4-3eb1-4e91-a096-965dc92a33f21bb8e3d3-b90b-4b97-be56-a3176dbfd0372016-11-29T18:41:352016-12-03T16:38:012772b496-48f7-4b4e-913a-92e583fc421c412a86f1-4df1-4017-8f43-d3f6ca5814c02017-07-18T16:56:522017-07-18T16:56:52412a86f1-4df1-4017-8f43-d3f6ca5814c0fc7e34d2-3b67-4709-a1fc-270ab32b64882017-07-18T16:57:482017-07-18T16:57:48NFE2L2/FXR activation leading to hepatic steatosisNRF2/FXR to steatosis<p>Michelle Angrish, Brian Chorley, U.S. EPA</p>
Under Development: Contributions and Comments WelcomeUnder Development1.29<p>Steatosis is a regulatory endpoint and has been used as an endpoint in many US EPA assessments, including IRIS assessments.</p>
adjacentNot SpecifiedNot SpecifiedadjacentNot SpecifiedNot SpecifiedadjacentNot SpecifiedNot SpecifiedadjacentNot SpecifiedNot SpecifiedadjacentNot SpecifiedNot SpecifiedadjacentNot SpecifiedNot SpecifiedadjacentNot SpecifiedNot SpecifiedadjacentNot SpecifiedNot Specifiednon-adjacentNot SpecifiedNot Specified2016-11-29T18:41:162023-04-29T16:02:56