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  • 1
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    Modulation of acetaminophen-induced hepatotoxicity by the xenobiotic receptor CAR (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-10-12
    Description: We have identified the xenobiotic receptor CAR (constitutive androstane receptor) as a key regulator of acetaminophen metabolism and hepatotoxicity. Known CAR activators as well as high doses of acetaminophen induced expression of three acetaminophen-metabolizing enzymes in wild-type but not in CAR null mice, and the CAR null mice were resistant to acetaminophen toxicity. Inhibition of CAR activity by administration of the inverse agonist ligand androstanol 1 hour after acetaminophen treatment blocked hepatotoxicity in wild type but not in CAR null mice. These results suggest an innovative therapeutic approach for treating the adverse effects of acetaminophen and potentially other hepatotoxic agents.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Jun -- Huang, Wendong -- Chua, Steven S -- Wei, Ping -- Moore, David D -- R01 DK46546/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2002 Oct 11;298(5592):422-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12376703" target="_blank"〉PubMed〈/a〉
    Keywords: Acetaminophen/metabolism/*toxicity ; Acetylcysteine/pharmacology ; Alanine Transaminase/blood ; Analgesics, Non-Narcotic/metabolism/toxicity ; Androstanols/pharmacology ; Animals ; Aryl Hydrocarbon Hydroxylases/genetics/metabolism ; Benzoquinones/metabolism ; Cytochrome P-450 CYP1A2/genetics/metabolism ; Cytochrome P-450 CYP2E1/genetics/metabolism ; Cytochrome P-450 CYP3A ; Cytochrome P-450 Enzyme System/genetics/metabolism ; Glutathione/metabolism ; Glutathione S-Transferase pi ; Glutathione Transferase/genetics/metabolism ; Humans ; Imines/metabolism ; Isoenzymes/genetics/metabolism ; Liver/*drug effects/*metabolism/pathology ; Mice ; Mice, Knockout ; Mice, Transgenic ; Oxidoreductases, N-Demethylating/genetics/metabolism ; Phenobarbital/pharmacology ; Pyridines/pharmacology ; RNA, Messenger/genetics/metabolism ; Receptors, Cytoplasmic and Nuclear/agonists/antagonists & ; inhibitors/genetics/*metabolism ; Time Factors ; Transcription Factors/agonists/antagonists & inhibitors/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Nutrient-sensing nuclear receptors coordinate autophagy (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-11-11
    Description: Autophagy is an evolutionarily conserved catabolic process that recycles nutrients upon starvation and maintains cellular energy homeostasis. Its acute regulation by nutrient-sensing signalling pathways is well described, but its longer-term transcriptional regulation is not. The nuclear receptors peroxisome proliferator-activated receptor-alpha (PPARalpha) and farnesoid X receptor (FXR) are activated in the fasted and fed liver, respectively. Here we show that both PPARalpha and FXR regulate hepatic autophagy in mice. Pharmacological activation of PPARalpha reverses the normal suppression of autophagy in the fed state, inducing autophagic lipid degradation, or lipophagy. This response is lost in PPARalpha knockout (Ppara(-/-), also known as Nr1c1(-/-)) mice, which are partially defective in the induction of autophagy by fasting. Pharmacological activation of the bile acid receptor FXR strongly suppresses the induction of autophagy in the fasting state, and this response is absent in FXR knockout (Fxr(-/-), also known as Nr1h4(-/-)) mice, which show a partial defect in suppression of hepatic autophagy in the fed state. PPARalpha and FXR compete for binding to shared sites in autophagic gene promoters, with opposite transcriptional outputs. These results reveal complementary, interlocking mechanisms for regulation of autophagy by nutrient status.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4267857/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4267857/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Jae Man -- Wagner, Martin -- Xiao, Rui -- Kim, Kang Ho -- Feng, Dan -- Lazar, Mitchell A -- Moore, David D -- DK43806/DK/NIDDK NIH HHS/ -- P30 DK019525/DK/NIDDK NIH HHS/ -- P30DX56338-05A2/PHS HHS/ -- P39CA125123-04/CA/NCI NIH HHS/ -- R01 DK049780/DK/NIDDK NIH HHS/ -- R01 DK49780/DK/NIDDK NIH HHS/ -- R37 DK043806/DK/NIDDK NIH HHS/ -- S10RR027783-01A1/RR/NCRR NIH HHS/ -- U54HD-07495-39/HD/NICHD NIH HHS/ -- England -- Nature. 2014 Dec 4;516(7529):112-5. doi: 10.1038/nature13961. Epub 2014 Nov 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030, USA. ; Division of Endocrinology, Diabetes, and Metabolism and the Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19014, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25383539" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autophagy/genetics/*physiology ; Cell Line ; Cells, Cultured ; Fasting/physiology ; Gene Expression Regulation ; Hepatocytes/metabolism ; Liver/cytology/*metabolism/ultrastructure ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Microtubule-Associated Proteins/genetics/metabolism ; PPAR alpha ; Receptors, Cytoplasmic and Nuclear/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    A nuclear-receptor-dependent phosphatidylcholine pathway with antidiabetic effects (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-05-27
    Description: Nuclear hormone receptors regulate diverse metabolic pathways and the orphan nuclear receptor LRH-1 (also known as NR5A2) regulates bile acid biosynthesis. Structural studies have identified phospholipids as potential LRH-1 ligands, but their functional relevance is unclear. Here we show that an unusual phosphatidylcholine species with two saturated 12 carbon fatty acid acyl side chains (dilauroyl phosphatidylcholine (DLPC)) is an LRH-1 agonist ligand in vitro. DLPC treatment induces bile acid biosynthetic enzymes in mouse liver, increases bile acid levels, and lowers hepatic triglycerides and serum glucose. DLPC treatment also decreases hepatic steatosis and improves glucose homeostasis in two mouse models of insulin resistance. Both the antidiabetic and lipotropic effects are lost in liver-specific Lrh-1 knockouts. These findings identify an LRH-1 dependent phosphatidylcholine signalling pathway that regulates bile acid metabolism and glucose homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3150801/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3150801/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Jae Man -- Lee, Yoon Kwang -- Mamrosh, Jennifer L -- Busby, Scott A -- Griffin, Patrick R -- Pathak, Manish C -- Ortlund, Eric A -- Moore, David D -- DK-079638/DK/NIDDK NIH HHS/ -- R01 CA134873/CA/NCI NIH HHS/ -- R01 DK068804/DK/NIDDK NIH HHS/ -- R01 DK083572/DK/NIDDK NIH HHS/ -- R01 DK083572-02/DK/NIDDK NIH HHS/ -- T32 DK007696/DK/NIDDK NIH HHS/ -- U54 MH084512/MH/NIMH NIH HHS/ -- England -- Nature. 2011 May 25;474(7352):506-10. doi: 10.1038/nature10111.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Developmental Biology, Baylor College of Medicine, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21614002" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bile Acids and Salts/biosynthesis/metabolism/pharmacology ; Blood Glucose/metabolism ; Cell Line ; Disease Models, Animal ; Fatty Liver/drug therapy/enzymology ; HeLa Cells ; Homeostasis/drug effects ; Humans ; Hypoglycemic Agents/pharmacology ; Insulin Resistance/physiology ; Ligands ; Lipogenesis/drug effects ; Liver/drug effects/enzymology/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Phosphatidylcholines/*metabolism/pharmacology ; Protein Binding ; Receptors, Cytoplasmic and Nuclear/agonists/deficiency/genetics/*metabolism ; Signal Transduction/drug effects ; Triglycerides/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Nuclear receptor-dependent bile acid signaling is required for normal liver regeneration (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-15
    Description: Liver mass depends on one or more unidentified humoral signals that drive regeneration when liver functional capacity is diminished. Bile acids are important liver products, and their levels are tightly regulated. Here, we identify a role for nuclear receptor-dependent bile acid signaling in normal liver regeneration. Elevated bile acid levels accelerate regeneration, and decreased levels inhibit liver regrowth, as does the absence of the primary nuclear bile acid receptor FXR. We propose that FXR activation by increased bile acid flux is a signal of decreased functional capacity of the liver. FXR, and possibly other nuclear receptors, may promote homeostasis not only by regulating expression of appropriate metabolic target genes but also by driving homeotrophic liver growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Wendong -- Ma, Ke -- Zhang, Jun -- Qatanani, Mohammed -- Cuvillier, James -- Liu, Jun -- Dong, Bingning -- Huang, Xiongfei -- Moore, David D -- R01 DK053366/DK/NIDDK NIH HHS/ -- U19 DK62434/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2006 Apr 14;312(5771):233-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16614213" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bile Acids and Salts/administration & dosage/blood/*metabolism ; Cell Count ; Cholesterol 7-alpha-Hydroxylase/genetics ; Cholestyramine Resin/administration & dosage/pharmacology ; Cholic Acid/administration & dosage ; Cytokines/genetics/metabolism ; DNA Replication ; DNA-Binding Proteins/genetics/*metabolism ; Diet ; Forkhead Transcription Factors/genetics/metabolism ; Gene Expression Regulation ; Genes, myc ; Growth Substances/genetics/metabolism ; Hepatectomy ; Hepatocytes/cytology ; Homeostasis ; Liver/cytology/metabolism/*physiology ; *Liver Regeneration ; Mice ; Mice, Knockout ; Proto-Oncogene Proteins c-myc/metabolism ; RNA, Messenger/genetics/metabolism ; Receptors, Cytoplasmic and Nuclear/genetics ; *Signal Transduction ; Transcription Factors/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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