PXR Ablation Alleviates Diet-Induced and Genetic Obesity and Insulin Resistance in Mice
The pregnane X receptor (PXR), along with its sister receptor constitutive androstane receptor (CAR), was initially characterized as a xenobiotic receptor that regulates drug metabolism. In this study, we have uncovered an unexpected endobiotic role of PXR in obesity and type 2 diabetes. PXR ablatio...
Saved in:
Published in | Diabetes (New York, N.Y.) Vol. 62; no. 6; pp. 1876 - 1887 |
---|---|
Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
Alexandria, VA
American Diabetes Association
01.06.2013
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Abstract | The pregnane X receptor (PXR), along with its sister receptor constitutive androstane receptor (CAR), was initially characterized as a xenobiotic receptor that regulates drug metabolism. In this study, we have uncovered an unexpected endobiotic role of PXR in obesity and type 2 diabetes. PXR ablation inhibited high-fat diet (HFD)–induced obesity, hepatic steatosis, and insulin resistance, which were accounted for by increased oxygen consumption, increased mitochondrial β-oxidation, inhibition of hepatic lipogenesis and inflammation, and sensitization of insulin signaling. In an independent model, introducing the PXR−/− allele into the ob/ob background also improved body composition and relieved the diabetic phenotype. The ob/ob mice deficient of PXR showed increased oxygen consumption and energy expenditure, as well as inhibition of gluconeogenesis and increased rate of glucose disposal during euglycemic clamp. Mechanistically, the metabolic benefits of PXR ablation were associated with the inhibition of c-Jun NH2-terminal kinase activation and downregulation of lipin-1, a novel PXR target gene. The metabolic benefit of PXR ablation was opposite to the reported prodiabetic effect of CAR ablation. Our results may help to establish PXR as a novel therapeutic target, and PXR antagonists may be used for the prevention and treatment of obesity and type 2 diabetes. |
---|---|
AbstractList | The pregnane X receptor (PXR), along with its sister receptor constitutive androstane receptor (CAR), was initially characterized as a xenobiotic receptor that regulates drug metabolism. In this study, we have uncovered an unexpected endobiotic role of PXR in obesity and type 2 diabetes. PXR ablation inhibited high-fat diet (HFD)--induced obesity, hepatic steatosis, and insulin resistance, which were accounted for by increased oxygen consumption, increased mitochondrial [beta]-oxidation, inhibition of hepatic lipogenesis and inflammation, and sensitization of insulin signaling. In an independent model, introducing the [PXR.sup.-/-] allele into the ob/ob background also improved body composition and relieved the diabetic phenotype. The ob/ob mice deficient of PXR showed increased oxygen consumption and energy expenditure, as well as inhibition of gluconeogenesis and increased rate of glucose disposal during euglycemic clamp. Mechanistically, the metabolic benefits of PXR ablation were associated with the inhibition of c-Jun N[H.sub.2]-terminal kinase activation and downregulation of lipin-1, a novel PXR target gene. The metabolic benefit of PXR ablation was opposite to the reported prodiabetic effect of CAR ablation. Our results may help to establish PXR as a novel therapeutic target, and PXR antagonists may be used for the prevention and treatment of obesity and type 2 diabetes. The pregnane X receptor (PXR), along with its sister receptor constitutive androstane receptor (CAR), was initially characterized as a xenobiotic receptor that regulates drug metabolism. In this study, we have uncovered an unexpected endobiotic role of PXR in obesity and type 2 diabetes. PXR ablation inhibited high-fat diet (HFD)-induced obesity, hepatic steatosis, and insulin resistance, which were accounted for by increased oxygen consumption, increased mitochondrial β-oxidation, inhibition of hepatic lipogenesis and inflammation, and sensitization of insulin signaling. In an independent model, introducing the PXR(-/-) allele into the ob/ob background also improved body composition and relieved the diabetic phenotype. The ob/ob mice deficient of PXR showed increased oxygen consumption and energy expenditure, as well as inhibition of gluconeogenesis and increased rate of glucose disposal during euglycemic clamp. Mechanistically, the metabolic benefits of PXR ablation were associated with the inhibition of c-Jun NH2-terminal kinase activation and downregulation of lipin-1, a novel PXR target gene. The metabolic benefit of PXR ablation was opposite to the reported prodiabetic effect of CAR ablation. Our results may help to establish PXR as a novel therapeutic target, and PXR antagonists may be used for the prevention and treatment of obesity and type 2 diabetes. The pregnane X receptor (PXR), along with its sister receptor constitutive androstane receptor (CAR), was initially characterized as a xenobiotic receptor that regulates drug metabolism. In this study, we have uncovered an unexpected endobiotic role of PXR in obesity and type 2 diabetes. PXR ablation inhibited high-fat diet (HFD)-induced obesity, hepatic steatosis, and insulin resistance, which were accounted for by increased oxygen consumption, increased mitochondrial β-oxidation, inhibition of hepatic lipogenesis and inflammation, and sensitization of insulin signaling. In an independent model, introducing the PXR(-/-) allele into the ob/ob background also improved body composition and relieved the diabetic phenotype. The ob/ob mice deficient of PXR showed increased oxygen consumption and energy expenditure, as well as inhibition of gluconeogenesis and increased rate of glucose disposal during euglycemic clamp. Mechanistically, the metabolic benefits of PXR ablation were associated with the inhibition of c-Jun NH2-terminal kinase activation and downregulation of lipin-1, a novel PXR target gene. The metabolic benefit of PXR ablation was opposite to the reported prodiabetic effect of CAR ablation. Our results may help to establish PXR as a novel therapeutic target, and PXR antagonists may be used for the prevention and treatment of obesity and type 2 diabetes.The pregnane X receptor (PXR), along with its sister receptor constitutive androstane receptor (CAR), was initially characterized as a xenobiotic receptor that regulates drug metabolism. In this study, we have uncovered an unexpected endobiotic role of PXR in obesity and type 2 diabetes. PXR ablation inhibited high-fat diet (HFD)-induced obesity, hepatic steatosis, and insulin resistance, which were accounted for by increased oxygen consumption, increased mitochondrial β-oxidation, inhibition of hepatic lipogenesis and inflammation, and sensitization of insulin signaling. In an independent model, introducing the PXR(-/-) allele into the ob/ob background also improved body composition and relieved the diabetic phenotype. The ob/ob mice deficient of PXR showed increased oxygen consumption and energy expenditure, as well as inhibition of gluconeogenesis and increased rate of glucose disposal during euglycemic clamp. Mechanistically, the metabolic benefits of PXR ablation were associated with the inhibition of c-Jun NH2-terminal kinase activation and downregulation of lipin-1, a novel PXR target gene. The metabolic benefit of PXR ablation was opposite to the reported prodiabetic effect of CAR ablation. Our results may help to establish PXR as a novel therapeutic target, and PXR antagonists may be used for the prevention and treatment of obesity and type 2 diabetes. The pregnane X receptor (PXR), along with its sister receptor constitutive androstane receptor (CAR), was initially characterized as a xenobiotic receptor that regulates drug metabolism. In this study, we have uncovered an unexpected endobiotic role of PXR in obesity and type 2 diabetes. PXR ablation inhibited high-fat diet (HFD)-induced obesity, hepatic steatosis, and insulin resistance, which were accounted for by increased oxygen consumption, increased mitochondrial [beta]-oxidation, inhibition of hepatic lipogenesis and inflammation, and sensitization of insulin signaling. In an independent model, introducing the PXR(-/-) allele into the ob/ob background also improved body composition and relieved the diabetic phenotype. The ob/ob mice deficient of PXR showed increased oxygen consumption and energy expenditure, as well as inhibition of gluconeogenesis and increased rate of glucose disposal during euglycemic clamp. Mechanistically, the metabolic benefits of PXR ablation were associated with the inhibition of c-Jun NH2-terminal kinase activation and downregulation of lipin-1, a novel PXR target gene. The metabolic benefit of PXR ablation was opposite to the reported prodiabetic effect of CAR ablation. Our results may help to establish PXR as a novel therapeutic target, and PXR antagonists may be used for the prevention and treatment of obesity and type 2 diabetes. The pregnane X receptor (PXR), along with its sister receptor constitutive androstane receptor (CAR), was initially characterized as a xenobiotic receptor that regulates drug metabolism. In this study, we have uncovered an unexpected endobiotic role of PXR in obesity and type 2 diabetes. PXR ablation inhibited high-fat diet (HFD)--induced obesity, hepatic steatosis, and insulin resistance, which were accounted for by increased oxygen consumption, increased mitochondrial β-oxidation, inhibition of hepatic lipogenesis and inflammation, and sensitization of insulin signaling. In an independent model, introducing the [PXR.sup.-/-] allele into the ob/ob background also improved body composition and relieved the diabetic phenotype. The ob/ob mice deficient of PXR showed increased oxygen consumption and energy expenditure, as well as inhibition of gluconeogenesis and increased rate of glucose disposal during euglycemic clamp. Mechanistically, the metabolic benefits of PXR ablation were associated with the inhibition of c-Jun N[H.sub.2]-terminal kinase activation and downregulation of lipin-1, a novel PXR target gene. The metabolic benefit of PXR ablation was opposite to the reported prodiabetic effect of CAR ablation. Our results may help to establish PXR as a novel therapeutic target, and PXR antagonists may be used for the prevention and treatment of obesity and type 2 diabetes. The pregnane X receptor (PXR), along with its sister receptor constitutive androstane receptor (CAR), was initially characterized as a xenobiotic receptor that regulates drug metabolism. In this study, we have uncovered an unexpected endobiotic role of PXR in obesity and type 2 diabetes. PXR ablation inhibited high-fat diet (HFD)–induced obesity, hepatic steatosis, and insulin resistance, which were accounted for by increased oxygen consumption, increased mitochondrial β-oxidation, inhibition of hepatic lipogenesis and inflammation, and sensitization of insulin signaling. In an independent model, introducing the PXR−/− allele into the ob/ob background also improved body composition and relieved the diabetic phenotype. The ob/ob mice deficient of PXR showed increased oxygen consumption and energy expenditure, as well as inhibition of gluconeogenesis and increased rate of glucose disposal during euglycemic clamp. Mechanistically, the metabolic benefits of PXR ablation were associated with the inhibition of c-Jun NH2-terminal kinase activation and downregulation of lipin-1, a novel PXR target gene. The metabolic benefit of PXR ablation was opposite to the reported prodiabetic effect of CAR ablation. Our results may help to establish PXR as a novel therapeutic target, and PXR antagonists may be used for the prevention and treatment of obesity and type 2 diabetes. The pregnane X receptor (PXR), along with its sister receptor constitutive androstane receptor (CAR), was initially characterized as a xenobiotic receptor that regulates drug metabolism. In this study, we have uncovered an unexpected endobiotic role of PXR in obesity and type 2 diabetes. PXR ablation inhibited high-fat diet (HFD)–induced obesity, hepatic steatosis, and insulin resistance, which were accounted for by increased oxygen consumption, increased mitochondrial β-oxidation, inhibition of hepatic lipogenesis and inflammation, and sensitization of insulin signaling. In an independent model, introducing the PXR −/− allele into the ob / ob background also improved body composition and relieved the diabetic phenotype. The ob / ob mice deficient of PXR showed increased oxygen consumption and energy expenditure, as well as inhibition of gluconeogenesis and increased rate of glucose disposal during euglycemic clamp. Mechanistically, the metabolic benefits of PXR ablation were associated with the inhibition of c-Jun NH 2 -terminal kinase activation and downregulation of lipin-1, a novel PXR target gene. The metabolic benefit of PXR ablation was opposite to the reported prodiabetic effect of CAR ablation. Our results may help to establish PXR as a novel therapeutic target, and PXR antagonists may be used for the prevention and treatment of obesity and type 2 diabetes. |
Audience | Professional |
Author | Ren, Songrong He, Jinhan Xie, Wen Xu, Meishu Stefanovic-Racic, Maja O'Doherty, Robert Martin Gao, Jie |
Author_xml | – sequence: 1 givenname: Jinhan surname: He fullname: He, Jinhan organization: Center for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania, Department of Pharmacy, West China Hospital, Sichuan University, Chengdu, Sichuan, China – sequence: 2 givenname: Jie surname: Gao fullname: Gao, Jie organization: Center for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania – sequence: 3 givenname: Meishu surname: Xu fullname: Xu, Meishu organization: Center for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania – sequence: 4 givenname: Songrong surname: Ren fullname: Ren, Songrong organization: Center for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania – sequence: 5 givenname: Maja surname: Stefanovic-Racic fullname: Stefanovic-Racic, Maja organization: Division of Endocrinology and Metabolism, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania – sequence: 6 givenname: Robert Martin surname: O'Doherty fullname: O'Doherty, Robert Martin organization: Division of Endocrinology and Metabolism, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania – sequence: 7 givenname: Wen surname: Xie fullname: Xie, Wen organization: Center for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania, Department of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, Pennsylvania |
BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27485196$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/23349477$$D View this record in MEDLINE/PubMed |
BookMark | eNp9klFv0zAQxy00xLrCA18ARUJI8JAtjmM7eUGqCpRKRUUTiL1ZjnMpnlxnxM7Evj2XUbZ1qpAfLJ9_d777-39CjnzngZCXNDvNGZNnTU3zlGasekImtGJVynJ5cUQmWTbGZSWPyUkIl1mWCVzPyDFmFVUh5YT8-Hpxnsxqp6PtfDJzDq6tjhCSDxZiuvTNYKBJtG-SBXiI1iTrGoKNN7expQ-Dsz45x1CI2htI8PTFGnhOnrbaBXix26fk-6eP3-af09V6sZzPVqkRUsQUdFHnJjclbdoGMtO2XOAFlQI4q0vd0KwqCsNynBCkKcu6kDnlOhe1Nk0u2JS8_1v3aqi30BjwsddOXfV2q_sb1Wmr9m-8_ak23bViQlCBYk3J212Bvvs1QIhqa4MB57SHbgiKMs6LEpWkiL5-hF52Q-9xPEWLXGRcVPwBtdEOlPVth--asaiaMZYLzrngSKUHqA1qjE3i77YWw3v86QEeVwNbaw4mvNtLQCbC77jRQwiqXKz-18yONR3aYQMKP2y-3udfPRT9Tu1_tkLgzQ7QwWjX9mgNG-45WZScVuK-SdN3IfTQ3iE0G6tJNVpbjdZG9uwRa2y8tS0qYd2BjD9Gx_VY |
CODEN | DIAEAZ |
CitedBy_id | crossref_primary_10_1002_tox_24094 crossref_primary_10_1038_ijo_2015_63 crossref_primary_10_1074_jbc_M113_494575 crossref_primary_10_1194_jlr_RA119000122 crossref_primary_10_1016_j_coph_2022_102314 crossref_primary_10_1016_j_molmet_2023_101779 crossref_primary_10_1093_toxsci_kfu083 crossref_primary_10_1124_mol_118_113647 crossref_primary_10_1093_toxsci_kfae047 crossref_primary_10_1111_iep_12306 crossref_primary_10_1152_ajprenal_00390_2017 crossref_primary_10_1016_j_bcp_2024_116309 crossref_primary_10_1016_j_fct_2023_113976 crossref_primary_10_1289_EHP9262 crossref_primary_10_1186_s12987_022_00375_3 crossref_primary_10_1038_s41598_019_53101_9 crossref_primary_10_3390_cells9112445 crossref_primary_10_1111_bcpt_13004 crossref_primary_10_1016_j_cbi_2019_05_038 crossref_primary_10_1016_j_toxlet_2024_07_003 crossref_primary_10_1155_2014_637027 crossref_primary_10_2174_1389200219666180918152241 crossref_primary_10_1210_me_2015_1292 crossref_primary_10_3390_cells11071125 crossref_primary_10_1016_j_bbagrm_2016_03_002 crossref_primary_10_1016_j_fct_2019_04_007 crossref_primary_10_1016_j_molpha_2024_100014 crossref_primary_10_1126_scitranslmed_aay7591 crossref_primary_10_1016_j_bbagrm_2016_02_015 crossref_primary_10_1016_j_molmet_2020_101119 crossref_primary_10_1016_j_apsb_2024_08_029 crossref_primary_10_3389_fimmu_2022_969399 crossref_primary_10_1007_s11883_015_0507_8 crossref_primary_10_3389_fendo_2019_00039 crossref_primary_10_1097_HC9_0000000000000343 crossref_primary_10_1530_JOE_17_0536 crossref_primary_10_1093_cdn_nzaa122 crossref_primary_10_1155_2021_6889533 crossref_primary_10_1016_j_bbagrm_2016_01_006 crossref_primary_10_1186_s12302_019_0195_z crossref_primary_10_1111_bph_15055 crossref_primary_10_1016_j_bbagrm_2016_04_010 crossref_primary_10_1080_17425255_2024_2309212 crossref_primary_10_1124_mol_117_108829 crossref_primary_10_1038_s41467_024_50198_z crossref_primary_10_1016_j_bcp_2017_07_019 crossref_primary_10_3390_ijms222312846 crossref_primary_10_1016_j_bcp_2020_114142 crossref_primary_10_1124_mol_116_104687 crossref_primary_10_3390_ijms25094836 crossref_primary_10_1111_bph_15433 crossref_primary_10_11131_2016_101198 crossref_primary_10_3390_ijms141122052 crossref_primary_10_1038_s41419_021_03768_8 crossref_primary_10_1038_srep40988 crossref_primary_10_1016_j_apsb_2018_09_007 crossref_primary_10_1016_j_apsb_2019_10_001 crossref_primary_10_3390_cells12232752 crossref_primary_10_3390_metabo11100706 crossref_primary_10_2174_1389200219666180611083155 crossref_primary_10_1016_j_jep_2023_116365 crossref_primary_10_3389_fphar_2024_1448744 crossref_primary_10_1016_j_jep_2024_119199 crossref_primary_10_1016_j_tox_2018_08_007 crossref_primary_10_1016_j_bcp_2022_115250 crossref_primary_10_1016_j_bcp_2015_11_023 crossref_primary_10_1016_j_taap_2014_06_019 crossref_primary_10_1016_j_bcp_2022_115012 crossref_primary_10_1042_BJ20150734 crossref_primary_10_1096_fj_202301126 crossref_primary_10_7717_peerj_7743 crossref_primary_10_1016_j_bcp_2019_04_008 crossref_primary_10_3389_fphar_2022_907271 crossref_primary_10_1021_acs_chemrestox_6b00186 crossref_primary_10_1111_liv_12578 crossref_primary_10_7554_eLife_37182 crossref_primary_10_1186_1476_511X_13_24 crossref_primary_10_1074_jbc_M117_815217 crossref_primary_10_1016_j_livres_2020_03_001 crossref_primary_10_2337_db16_1225 crossref_primary_10_1016_j_bcp_2013_03_016 crossref_primary_10_1016_j_livres_2018_12_002 crossref_primary_10_1124_mol_114_097287 crossref_primary_10_1016_j_bcp_2021_114698 crossref_primary_10_1097_MOG_0000000000000816 crossref_primary_10_1210_me_2014_1355 crossref_primary_10_3390_md17100554 crossref_primary_10_1007_s00204_014_1348_x crossref_primary_10_1016_j_bcp_2018_01_001 crossref_primary_10_1016_j_biopha_2024_116341 crossref_primary_10_1016_j_bbadis_2021_166101 crossref_primary_10_1016_j_jlr_2021_100051 crossref_primary_10_1124_dmd_123_001311 crossref_primary_10_1124_dmd_122_000862 crossref_primary_10_1124_mol_113_085753 crossref_primary_10_1371_journal_pone_0087697 crossref_primary_10_1016_j_bbagrm_2016_03_012 crossref_primary_10_1124_dmd_121_000415 crossref_primary_10_1038_nrendo_2013_226 crossref_primary_10_3390_cells10123550 crossref_primary_10_1002_med_21648 crossref_primary_10_1002_jcp_24838 crossref_primary_10_1016_j_mce_2019_02_002 crossref_primary_10_1016_j_metabol_2024_156054 crossref_primary_10_1038_s41467_025_56642_y crossref_primary_10_4331_wjbc_v8_i2_108 crossref_primary_10_1007_s00204_024_03942_9 crossref_primary_10_1016_j_molmet_2020_100994 crossref_primary_10_1074_jbc_M113_535914 crossref_primary_10_1016_j_bcp_2014_03_019 crossref_primary_10_1124_dmd_118_081042 crossref_primary_10_3390_ijerph17249403 crossref_primary_10_1515_mr_2022_0032 crossref_primary_10_1016_j_obmed_2020_100197 crossref_primary_10_1016_j_envpol_2021_117855 crossref_primary_10_1016_j_toxlet_2022_11_021 crossref_primary_10_3390_foods11172543 crossref_primary_10_3390_ijms20153767 |
Cites_doi | 10.1016/j.tips.2012.03.003 10.1016/j.cmet.2009.01.007 10.1371/journal.pone.0038734 10.1074/jbc.M109.016808 10.1074/jbc.M610072200 10.1194/jlr.M800204-JLR200 10.1002/hep.24140 10.1124/dmd.30.7.814 10.1016/S0092-8674(00)80900-9 10.1002/j.1552-4604.1982.tb02652.x 10.1038/nature01137 10.1056/NEJM196907102810208 10.1093/toxsci/kfs211 10.1016/S0022-2275(20)30474-0 10.1038/sj.onc.1209788 10.1124/dmd.30.7.795 10.1124/mol.111.071787 10.1124/dmd.110.035568 10.1124/mol.108.049437 10.1097/MOL.0b013e32834b4994 10.1074/jbc.M511116200 10.1042/BJ20070481 10.1073/pnas.0909731106 10.7326/0003-4819-118-7-199304010-00008 10.1038/35019116 10.1002/cncr.20071 10.1016/j.bmcl.2008.06.018 10.1101/gad.12.20.3195 10.1126/scitranslmed.3001007 10.1111/j.1464-5491.1991.tb01539.x 10.1128/MCB.24.18.7931-7940.2004 10.2337/db11-1152 10.1210/me.2007-0218 10.1074/jbc.M405423200 10.3109/00498254.2011.569773 10.1001/jama.286.16.1945 10.1634/theoncologist.12-1-99 |
ClassificationCodes | 2831720 |
ContentType | Journal Article |
Copyright | 2014 INIST-CNRS COPYRIGHT 2013 American Diabetes Association COPYRIGHT 2013 American Diabetes Association Copyright American Diabetes Association Jun 2013 2013 by the American Diabetes Association. 2013 |
Copyright_xml | – notice: 2014 INIST-CNRS – notice: COPYRIGHT 2013 American Diabetes Association – notice: COPYRIGHT 2013 American Diabetes Association – notice: Copyright American Diabetes Association Jun 2013 – notice: 2013 by the American Diabetes Association. 2013 |
DBID | AAYXX CITATION IQODW CGR CUY CVF ECM EIF NPM 8GL 3V. 7RV 7X7 7XB 88E 88I 8AF 8AO 8C1 8FE 8FH 8FI 8FJ 8FK 8G5 ABUWG AFKRA AZQEC BBNVY BEC BENPR BHPHI CCPQU DWQXO FYUFA GHDGH GNUQQ GUQSH HCIFZ K9- K9. KB0 LK8 M0R M0S M1P M2O M2P M7P MBDVC NAPCQ PHGZM PHGZT PJZUB PKEHL PPXIY PQEST PQGLB PQQKQ PQUKI PRINS Q9U S0X 7X8 5PM |
DOI | 10.2337/db12-1039 |
DatabaseName | CrossRef Pascal-Francis Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed Gale In Context: High School ProQuest Central (Corporate) Nursing & Allied Health Database Health & Medical Collection ProQuest Central (purchase pre-March 2016) Medical Database (Alumni Edition) Science Database (Alumni Edition) STEM Database ProQuest Pharma Collection Public Health Database ProQuest SciTech Collection ProQuest Natural Science Journals Hospital Premium Collection Hospital Premium Collection (Alumni Edition) ProQuest Central (Alumni) (purchase pre-March 2016) ProQuest Research Library ProQuest Central (Alumni) ProQuest Central UK/Ireland ProQuest Central Essentials Biological Science Database eLibrary Curriculum ProQuest Central Natural Science Collection ProQuest One Community College ProQuest Central Korea Health Research Premium Collection Health Research Premium Collection (Alumni) ProQuest Central Student ProQuest Research Library SciTech Premium Collection Consumer Health Database (Alumni Edition) ProQuest Health & Medical Complete (Alumni) Nursing & Allied Health Database (Alumni Edition) ProQuest Biological Science Collection Consumer Health Database ProQuest Health & Medical Collection PML(ProQuest Medical Library) Research Library Science Database Biological Science Database Research Library (Corporate) Nursing & Allied Health Premium ProQuest Central Premium ProQuest One Academic ProQuest Health & Medical Research Collection ProQuest One Academic Middle East (New) ProQuest One Health & Nursing ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Applied & Life Sciences ProQuest One Academic ProQuest One Academic UKI Edition ProQuest Central China ProQuest Central Basic SIRS Editorial MEDLINE - Academic PubMed Central (Full Participant titles) |
DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) Research Library Prep ProQuest Central Student ProQuest Central Essentials elibrary ProQuest AP Science SciTech Premium Collection ProQuest Central China ProQuest One Applied & Life Sciences Health Research Premium Collection Natural Science Collection Health & Medical Research Collection Biological Science Collection ProQuest Central (New) ProQuest Medical Library (Alumni) ProQuest Science Journals (Alumni Edition) ProQuest Biological Science Collection ProQuest Family Health ProQuest One Academic Eastern Edition ProQuest Hospital Collection Health Research Premium Collection (Alumni) Biological Science Database ProQuest Hospital Collection (Alumni) Nursing & Allied Health Premium ProQuest Health & Medical Complete ProQuest One Academic UKI Edition ProQuest Nursing & Allied Health Source (Alumni) ProQuest One Academic ProQuest One Academic (New) ProQuest One Academic Middle East (New) SIRS Editorial ProQuest Health & Medical Complete (Alumni) ProQuest Central (Alumni Edition) ProQuest One Community College ProQuest One Health & Nursing Research Library (Alumni Edition) ProQuest Natural Science Collection ProQuest Pharma Collection ProQuest Family Health (Alumni Edition) ProQuest Central ProQuest Health & Medical Research Collection Health and Medicine Complete (Alumni Edition) ProQuest Central Korea ProQuest Research Library ProQuest Public Health ProQuest Central Basic ProQuest Science Journals ProQuest Nursing & Allied Health Source ProQuest SciTech Collection ProQuest Medical Library ProQuest Central (Alumni) MEDLINE - Academic |
DatabaseTitleList | MEDLINE MEDLINE - Academic Research Library Prep CrossRef |
Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database – sequence: 3 dbid: BENPR name: ProQuest Central - New (Subscription) url: https://www.proquest.com/central sourceTypes: Aggregation Database |
DeliveryMethod | fulltext_linktorsrc |
Discipline | Medicine |
EISSN | 1939-327X |
EndPage | 1887 |
ExternalDocumentID | PMC3661619 3048635141 A332655565 23349477 27485196 10_2337_db12_1039 |
Genre | Research Support, Non-U.S. Gov't Journal Article Research Support, N.I.H., Extramural |
GrantInformation_xml | – fundername: NIDDK NIH HHS grantid: R01 DK083952 – fundername: NIEHS NIH HHS grantid: ES-019629 – fundername: NIEHS NIH HHS grantid: R21 ES019629 – fundername: NCATS NIH HHS grantid: UL1 TR000005 – fundername: NIDDK NIH HHS grantid: DK-083952 – fundername: NIDDK NIH HHS grantid: R01 DK072162 – fundername: NIDDK NIH HHS grantid: R01 DK058855 |
GroupedDBID | --- .55 .XZ 08P 0R~ 18M 29F 2WC 354 4.4 53G 5GY 5RE 5RS 5VS 6PF 7RV 7X7 88E 88I 8AF 8AO 8C1 8FE 8FH 8FI 8FJ 8G5 8GL 8R4 8R5 AAFWJ AAKAS AAQQT AAWTL AAYEP AAYOK AAYXX ABOCM ABUWG ACGFO ACGOD ACPRK ADBBV ADGHP ADZCM AEGXH AENEX AERZD AFKRA AHMBA AIAGR AIZAD ALIPV ALMA_UNASSIGNED_HOLDINGS AZQEC BAWUL BBNVY BCU BEC BENPR BES BHPHI BKEYQ BKNYI BPHCQ BTFSW BVXVI CCPQU CITATION CS3 DIK DU5 DWQXO E3Z EBS EDB EJD EMOBN EX3 F5P FRP FYUFA GICCO GNUQQ GUQSH GX1 H13 HCIFZ HMCUK HZ~ IAG IAO IEA IHR INH INR IOF IPO ITC K-O K2M K9- KQ8 L7B LK8 M0R M1P M2O M2P M2Q M5~ M7P NAPCQ O5R O5S O9- OB3 OHH OK1 OVD P2P PCD PHGZM PHGZT PQQKQ PROAC PSQYO Q2X RHI RPM S0X SJFOW SJN SV3 TDI TEORI TR2 UKHRP VVN W8F WH7 WOQ WOW X7M YFH YHG YOC ZY1 ~KM .GJ 1CY 8F7 AAYJJ AFFNX AI. BCR BLC C1A H~9 IQODW J5H MVM N4W PEA PJZUB PPXIY PQGLB VH1 XOL YQJ ZGI ZXP CGR CUY CVF ECM EIF NPM PMFND 3V. 7XB 8FK K9. MBDVC PKEHL PQEST PQUKI PRINS Q9U 7X8 5PM |
ID | FETCH-LOGICAL-c676t-ea4b2c2c81dfde0cff56676176e53b8ad10944c32b12e7c88b47215a26bacd263 |
IEDL.DBID | 7X7 |
ISSN | 0012-1797 1939-327X |
IngestDate | Thu Aug 21 18:36:23 EDT 2025 Fri Jul 11 15:51:49 EDT 2025 Fri Jul 25 19:37:12 EDT 2025 Tue Jun 17 20:55:16 EDT 2025 Thu Jun 12 23:01:04 EDT 2025 Tue Jun 10 20:19:44 EDT 2025 Fri Jun 27 03:55:29 EDT 2025 Tue Jun 10 19:50:47 EDT 2025 Mon Jul 21 06:03:21 EDT 2025 Mon Jul 21 09:17:28 EDT 2025 Thu Apr 24 22:53:30 EDT 2025 Tue Jul 01 03:04:10 EDT 2025 |
IsDoiOpenAccess | true |
IsOpenAccess | true |
IsPeerReviewed | true |
IsScholarly | true |
Issue | 6 |
Keywords | Endocrinopathy Obesity Diabetes mellitus Rodentia Nutrition disorder Metabolic diseases Ablation Feeding Target tissue resistance Vertebrata Mammalia Diet Mouse Animal Genetics Insulin resistance Nutritional status |
Language | English |
License | CC BY 4.0 Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details. |
LinkModel | DirectLink |
MergedId | FETCHMERGED-LOGICAL-c676t-ea4b2c2c81dfde0cff56676176e53b8ad10944c32b12e7c88b47215a26bacd263 |
Notes | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-General Information-1 content type line 14 ObjectType-Feature-3 ObjectType-Article-1 ObjectType-Feature-2 content type line 23 |
OpenAccessLink | https://pubmed.ncbi.nlm.nih.gov/PMC3661619 |
PMID | 23349477 |
PQID | 1426056951 |
PQPubID | 34443 |
PageCount | 12 |
ParticipantIDs | pubmedcentral_primary_oai_pubmedcentral_nih_gov_3661619 proquest_miscellaneous_1355480011 proquest_journals_1426056951 gale_infotracmisc_A332655565 gale_infotracgeneralonefile_A332655565 gale_infotracacademiconefile_A332655565 gale_incontextgauss_8GL_A332655565 gale_incontextcollege_GICCO_A332655565 pubmed_primary_23349477 pascalfrancis_primary_27485196 crossref_primary_10_2337_db12_1039 crossref_citationtrail_10_2337_db12_1039 |
ProviderPackageCode | CITATION AAYXX |
PublicationCentury | 2000 |
PublicationDate | 2013-06-01 |
PublicationDateYYYYMMDD | 2013-06-01 |
PublicationDate_xml | – month: 06 year: 2013 text: 2013-06-01 day: 01 |
PublicationDecade | 2010 |
PublicationPlace | Alexandria, VA |
PublicationPlace_xml | – name: Alexandria, VA – name: United States – name: New York |
PublicationTitle | Diabetes (New York, N.Y.) |
PublicationTitleAlternate | Diabetes |
PublicationYear | 2013 |
Publisher | American Diabetes Association |
Publisher_xml | – name: American Diabetes Association |
References | Carter (2022031210230197400_B14) 1981; 38 Lindley (2022031210230197400_B9) 2002; 30 Gao (2022031210230197400_B27) 2012; 61 Hirosumi (2022031210230197400_B30) 2002; 420 Ekins (2022031210230197400_B39) 2008; 74 Kliewer (2022031210230197400_B2) 1998; 92 Peters (2022031210230197400_B15) 1969; 281 Bou Khalil (2022031210230197400_B32) 2009; 50 Chen (2022031210230197400_B29) 2002; 43 al-Rubeaan (2022031210230197400_B12) 1991; 8 Gao (2022031210230197400_B28) 2009; 284 Cheng (2022031210230197400_B24) 2012; 129 Pandit (2022031210230197400_B6) 1993; 118 Huang (2022031210230197400_B34) Kodama (2022031210230197400_B20) 2004; 24 Xie (2022031210230197400_B26) 2000; 406 Preiss (2022031210230197400_B11) 2011; 22 Gao (2022031210230197400_B23) 2010; 38 Ma (2022031210230197400_B25) 2012; 7 Vallerie (2022031210230197400_B31) 2010; 2 2022031210230197400_B3 Venkatesh (2022031210230197400_B37) 2011; 80 Zhou (2022031210230197400_B19) 2006; 281 Luo (2022031210230197400_B8) 2002; 30 Suvannasankha (2022031210230197400_B16) 2007; 12 Orellana-Gavaldà (2022031210230197400_B35) 2011; 53 Das (2022031210230197400_B38) 2008; 18 Ryu (2022031210230197400_B33) 2009; 9 Howe (2022031210230197400_B7) 2011; 41 Weiser (2022031210230197400_B17) 2004; 100 Nakamura (2022031210230197400_B18) 2007; 282 Wang (2022031210230197400_B41) 2008; 22 Blumberg (2022031210230197400_B1) 1998; 12 Luna (2022031210230197400_B5) 2001; 286 Kodama (2022031210230197400_B21) 2007; 407 Dong (2022031210230197400_B36) 2009; 106 Huang (2022031210230197400_B40) 2007; 26 Takasu (2022031210230197400_B10) 1982; 125 Banner (2022031210230197400_B13) 1982; 22 Bhalla (2022031210230197400_B22) 2004; 279 Cheng (2022031210230197400_B4) 2012; 33 20736325 - Drug Metab Dispos. 2010 Dec;38(12):2091-5 8442624 - Ann Intern Med. 1993 Apr 1;118(7):529-39 19254569 - Cell Metab. 2009 Mar;9(3):240-51 9489701 - Cell. 1998 Jan 9;92(1):73-82 21295138 - Biochim Biophys Acta. 2011 Aug;1812(8):956-63 12065438 - Drug Metab Dispos. 2002 Jul;30(7):795-804 21319201 - Hepatology. 2011 Mar;53(3):821-32 21897230 - Curr Opin Lipidol. 2011 Dec;22(6):460-6 17267396 - J Biol Chem. 2007 Mar 30;282(13):9768-76 12447443 - Nature. 2002 Nov 21;420(6913):333-6 11667913 - JAMA. 2001 Oct 24-31;286(16):1945-8 17635106 - Biochem J. 2007 Nov 1;407(3):373-81 7039435 - Am Rev Respir Dis. 1982 Jan;125(1):23-7 1838051 - Diabet Med. 1991 Dec;8(10):968-70 15022284 - Cancer. 2004 Mar 15;100(6):1179-85 7040499 - J Clin Pharmacol. 1982 Feb-Mar;22(2-3):79-81 17227904 - Oncologist. 2007 Jan;12(1):99-106 21123811 - Sci Transl Med. 2010 Dec 1;2(60):60rv5 18583127 - Bioorg Med Chem Lett. 2008 Jul 15;18(14):3974-7 16556603 - J Biol Chem. 2006 May 26;281(21):15013-20 15322103 - J Biol Chem. 2004 Oct 22;279(43):45139-47 18769019 - J Lipid Res. 2009 Jan;50(1):47-58 12065440 - Drug Metab Dispos. 2002 Jul;30(7):814-22 22009939 - FASEB J. 2012 Feb;26(2):628-38 19617349 - J Biol Chem. 2009 Sep 18;284(38):25984-92 19850873 - Proc Natl Acad Sci U S A. 2009 Nov 3;106(44):18831-6 21476904 - Xenobiotica. 2011 Jul;41(7):519-29 7294047 - Am J Hosp Pharm. 1981 Oct;38(10):1508-12 18096694 - Mol Endocrinol. 2008 Apr;22(4):838-57 15340055 - Mol Cell Biol. 2004 Sep;24(18):7931-40 5784786 - N Engl J Med. 1969 Jul 10;281(2):91-2 10935643 - Nature. 2000 Jul 27;406(6794):435-9 22723881 - PLoS One. 2012;7(6):e38734 9784494 - Genes Dev. 1998 Oct 15;12(20):3195-205 18579710 - Mol Pharmacol. 2008 Sep;74(3):662-72 16819505 - Oncogene. 2007 Jan 11;26(2):258-68 21464197 - Mol Pharmacol. 2011 Jul;80(1):124-35 22609277 - Trends Pharmacol Sci. 2012 Jun;33(6):323-30 22438574 - Diabetes. 2012 Jun;61(6):1543-51 22790967 - Toxicol Sci. 2012 Oct;129(2):456-68 12032175 - J Lipid Res. 2002 Jun;43(6):986-9 |
References_xml | – volume: 33 start-page: 323 year: 2012 ident: 2022031210230197400_B4 article-title: Pregnane X receptor as a target for treatment of inflammatory bowel disorders publication-title: Trends Pharmacol Sci doi: 10.1016/j.tips.2012.03.003 – volume: 9 start-page: 240 year: 2009 ident: 2022031210230197400_B33 article-title: TORC2 regulates hepatic insulin signaling via a mammalian phosphatidic acid phosphatase, LIPIN1 publication-title: Cell Metab doi: 10.1016/j.cmet.2009.01.007 – ident: 2022031210230197400_B3 – volume: 7 start-page: e38734 year: 2012 ident: 2022031210230197400_B25 article-title: Activation of pregnane X receptor by pregnenolone 16 α-carbonitrile prevents high-fat diet-induced obesity in AKR/J mice publication-title: PLoS ONE doi: 10.1371/journal.pone.0038734 – volume: 284 start-page: 25984 year: 2009 ident: 2022031210230197400_B28 article-title: The constitutive androstane receptor is an anti-obesity nuclear receptor that improves insulin sensitivity publication-title: J Biol Chem doi: 10.1074/jbc.M109.016808 – volume: 282 start-page: 9768 year: 2007 ident: 2022031210230197400_B18 article-title: Nuclear pregnane X receptor cross-talk with FoxA2 to mediate drug-induced regulation of lipid metabolism in fasting mouse liver publication-title: J Biol Chem doi: 10.1074/jbc.M610072200 – volume: 50 start-page: 47 year: 2009 ident: 2022031210230197400_B32 article-title: The level and compartmentalization of phosphatidate phosphatase-1 (lipin-1) control the assembly and secretion of hepatic VLDL publication-title: J Lipid Res doi: 10.1194/jlr.M800204-JLR200 – volume: 53 start-page: 821 year: 2011 ident: 2022031210230197400_B35 article-title: Molecular therapy for obesity and diabetes based on a long-term increase in hepatic fatty-acid oxidation publication-title: Hepatology doi: 10.1002/hep.24140 – volume: 30 start-page: 814 year: 2002 ident: 2022031210230197400_B9 article-title: The effect of cyclophosphamide with and without dexamethasone on cytochrome P450 3A4 and 2B6 in human hepatocytes publication-title: Drug Metab Dispos doi: 10.1124/dmd.30.7.814 – volume: 92 start-page: 73 year: 1998 ident: 2022031210230197400_B2 article-title: An orphan nuclear receptor activated by pregnanes defines a novel steroid signaling pathway publication-title: Cell doi: 10.1016/S0092-8674(00)80900-9 – volume: 125 start-page: 23 year: 1982 ident: 2022031210230197400_B10 article-title: Rifampicin-induced early phase hyperglycemia in humans publication-title: Am Rev Respir Dis – volume: 22 start-page: 79 year: 1982 ident: 2022031210230197400_B13 article-title: Effects of single large doses of phenytoin on glucose homeostasis—a preliminary report publication-title: J Clin Pharmacol doi: 10.1002/j.1552-4604.1982.tb02652.x – ident: 2022031210230197400_B34 article-title: Sustained activation of CptR{alpha} by endogenous ligands increases hepatic fatty acid oxidation and prevents obesity in ob/ob mice publication-title: FASEB J – volume: 420 start-page: 333 year: 2002 ident: 2022031210230197400_B30 article-title: A central role for JNK in obesity and insulin resistance publication-title: Nature doi: 10.1038/nature01137 – volume: 281 start-page: 91 year: 1969 ident: 2022031210230197400_B15 article-title: Hyperglycemia with relative hypoinsulinemia in diphenylhydantoin toxicity publication-title: N Engl J Med doi: 10.1056/NEJM196907102810208 – volume: 129 start-page: 456 year: 2012 ident: 2022031210230197400_B24 article-title: Chronic exposure to rifaximin causes hepatic steatosis in pregnane X receptor-humanized mice publication-title: Toxicol Sci doi: 10.1093/toxsci/kfs211 – volume: 43 start-page: 986 year: 2002 ident: 2022031210230197400_B29 article-title: Determination of adipocyte size by computer image analysis publication-title: J Lipid Res doi: 10.1016/S0022-2275(20)30474-0 – volume: 26 start-page: 258 year: 2007 ident: 2022031210230197400_B40 article-title: Inhibition of drug metabolism by blocking the activation of nuclear receptors by ketoconazole publication-title: Oncogene doi: 10.1038/sj.onc.1209788 – volume: 30 start-page: 795 year: 2002 ident: 2022031210230197400_B8 article-title: CYP3A4 induction by drugs: correlation between a pregnane X receptor reporter gene assay and CYP3A4 expression in human hepatocytes publication-title: Drug Metab Dispos doi: 10.1124/dmd.30.7.795 – volume: 38 start-page: 1508 year: 1981 ident: 2022031210230197400_B14 article-title: Phenytoin-induced hyperglycemia publication-title: Am J Hosp Pharm – volume: 80 start-page: 124 year: 2011 ident: 2022031210230197400_B37 article-title: In vivo and in vitro characterization of a first-in-class novel azole analog that targets pregnane X receptor activation publication-title: Mol Pharmacol doi: 10.1124/mol.111.071787 – volume: 38 start-page: 2091 year: 2010 ident: 2022031210230197400_B23 article-title: Pregnane X receptor and constitutive androstane receptor at the crossroads of drug metabolism and energy metabolism publication-title: Drug Metab Dispos doi: 10.1124/dmd.110.035568 – volume: 74 start-page: 662 year: 2008 ident: 2022031210230197400_B39 article-title: Computational discovery of novel low micromolar human pregnane X receptor antagonists publication-title: Mol Pharmacol doi: 10.1124/mol.108.049437 – volume: 22 start-page: 460 year: 2011 ident: 2022031210230197400_B11 article-title: Statins and the risk of new-onset diabetes: a review of recent evidence publication-title: Curr Opin Lipidol doi: 10.1097/MOL.0b013e32834b4994 – volume: 281 start-page: 15013 year: 2006 ident: 2022031210230197400_B19 article-title: A novel pregnane X receptor-mediated and sterol regulatory element-binding protein-independent lipogenic pathway publication-title: J Biol Chem doi: 10.1074/jbc.M511116200 – volume: 407 start-page: 373 year: 2007 ident: 2022031210230197400_B21 article-title: Human nuclear pregnane X receptor cross-talk with CREB to repress cAMP activation of the glucose-6-phosphatase gene publication-title: Biochem J doi: 10.1042/BJ20070481 – volume: 106 start-page: 18831 year: 2009 ident: 2022031210230197400_B36 article-title: Activation of nuclear receptor CAR ameliorates diabetes and fatty liver disease publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.0909731106 – volume: 118 start-page: 529 year: 1993 ident: 2022031210230197400_B6 article-title: Drug-induced disorders of glucose tolerance publication-title: Ann Intern Med doi: 10.7326/0003-4819-118-7-199304010-00008 – volume: 406 start-page: 435 year: 2000 ident: 2022031210230197400_B26 article-title: Humanized xenobiotic response in mice expressing nuclear receptor SXR publication-title: Nature doi: 10.1038/35019116 – volume: 100 start-page: 1179 year: 2004 ident: 2022031210230197400_B17 article-title: Relation between the duration of remission and hyperglycemia during induction chemotherapy for acute lymphocytic leukemia with a hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone/methotrexate-cytarabine regimen publication-title: Cancer doi: 10.1002/cncr.20071 – volume: 18 start-page: 3974 year: 2008 ident: 2022031210230197400_B38 article-title: Synthesis of novel ketoconazole derivatives as inhibitors of the human pregnane X receptor (PXR; NR1I2; also termed SXR, PAR) publication-title: Bioorg Med Chem Lett doi: 10.1016/j.bmcl.2008.06.018 – volume: 12 start-page: 3195 year: 1998 ident: 2022031210230197400_B1 article-title: SXR, a novel steroid and xenobiotic-sensing nuclear receptor publication-title: Genes Dev doi: 10.1101/gad.12.20.3195 – volume: 2 start-page: rv5 year: 2010 ident: 2022031210230197400_B31 article-title: The role of JNK proteins in metabolism publication-title: Sci Transl Med doi: 10.1126/scitranslmed.3001007 – volume: 8 start-page: 968 year: 1991 ident: 2022031210230197400_B12 article-title: Phenytoin-induced insulin insensitivity publication-title: Diabet Med doi: 10.1111/j.1464-5491.1991.tb01539.x – volume: 24 start-page: 7931 year: 2004 ident: 2022031210230197400_B20 article-title: Nuclear receptors CAR and PXR cross talk with FOXO1 to regulate genes that encode drug-metabolizing and gluconeogenic enzymes publication-title: Mol Cell Biol doi: 10.1128/MCB.24.18.7931-7940.2004 – volume: 61 start-page: 1543 year: 2012 ident: 2022031210230197400_B27 article-title: Sex-specific effect of estrogen sulfotransferase on mouse models of type 2 diabetes publication-title: Diabetes doi: 10.2337/db11-1152 – volume: 22 start-page: 838 year: 2008 ident: 2022031210230197400_B41 article-title: The phytoestrogen coumestrol is a naturally occurring antagonist of the human pregnane X receptor publication-title: Mol Endocrinol doi: 10.1210/me.2007-0218 – volume: 279 start-page: 45139 year: 2004 ident: 2022031210230197400_B22 article-title: Ligand-activated pregnane X receptor interferes with HNF-4 signaling by targeting a common coactivator PGC-1alpha. Functional implications in hepatic cholesterol and glucose metabolism publication-title: J Biol Chem doi: 10.1074/jbc.M405423200 – volume: 41 start-page: 519 year: 2011 ident: 2022031210230197400_B7 article-title: The statin class of HMG-CoA reductase inhibitors demonstrate differential activation of the nuclear receptors PXR, CAR and FXR, as well as their downstream target genes publication-title: Xenobiotica doi: 10.3109/00498254.2011.569773 – volume: 286 start-page: 1945 year: 2001 ident: 2022031210230197400_B5 article-title: Drug-induced hyperglycemia publication-title: JAMA doi: 10.1001/jama.286.16.1945 – volume: 12 start-page: 99 year: 2007 ident: 2022031210230197400_B16 article-title: Final report of toxicity and efficacy of a phase II study of oral cyclophosphamide, thalidomide, and prednisone for patients with relapsed or refractory multiple myeloma: a Hoosier Oncology Group Trial, HEM01-21 publication-title: Oncologist doi: 10.1634/theoncologist.12-1-99 – reference: 17267396 - J Biol Chem. 2007 Mar 30;282(13):9768-76 – reference: 22723881 - PLoS One. 2012;7(6):e38734 – reference: 18096694 - Mol Endocrinol. 2008 Apr;22(4):838-57 – reference: 11667913 - JAMA. 2001 Oct 24-31;286(16):1945-8 – reference: 9784494 - Genes Dev. 1998 Oct 15;12(20):3195-205 – reference: 15022284 - Cancer. 2004 Mar 15;100(6):1179-85 – reference: 18583127 - Bioorg Med Chem Lett. 2008 Jul 15;18(14):3974-7 – reference: 22009939 - FASEB J. 2012 Feb;26(2):628-38 – reference: 21464197 - Mol Pharmacol. 2011 Jul;80(1):124-35 – reference: 19254569 - Cell Metab. 2009 Mar;9(3):240-51 – reference: 12065438 - Drug Metab Dispos. 2002 Jul;30(7):795-804 – reference: 17635106 - Biochem J. 2007 Nov 1;407(3):373-81 – reference: 19850873 - Proc Natl Acad Sci U S A. 2009 Nov 3;106(44):18831-6 – reference: 12065440 - Drug Metab Dispos. 2002 Jul;30(7):814-22 – reference: 9489701 - Cell. 1998 Jan 9;92(1):73-82 – reference: 19617349 - J Biol Chem. 2009 Sep 18;284(38):25984-92 – reference: 12032175 - J Lipid Res. 2002 Jun;43(6):986-9 – reference: 10935643 - Nature. 2000 Jul 27;406(6794):435-9 – reference: 16556603 - J Biol Chem. 2006 May 26;281(21):15013-20 – reference: 12447443 - Nature. 2002 Nov 21;420(6913):333-6 – reference: 15322103 - J Biol Chem. 2004 Oct 22;279(43):45139-47 – reference: 7039435 - Am Rev Respir Dis. 1982 Jan;125(1):23-7 – reference: 21476904 - Xenobiotica. 2011 Jul;41(7):519-29 – reference: 1838051 - Diabet Med. 1991 Dec;8(10):968-70 – reference: 17227904 - Oncologist. 2007 Jan;12(1):99-106 – reference: 21319201 - Hepatology. 2011 Mar;53(3):821-32 – reference: 7294047 - Am J Hosp Pharm. 1981 Oct;38(10):1508-12 – reference: 16819505 - Oncogene. 2007 Jan 11;26(2):258-68 – reference: 20736325 - Drug Metab Dispos. 2010 Dec;38(12):2091-5 – reference: 7040499 - J Clin Pharmacol. 1982 Feb-Mar;22(2-3):79-81 – reference: 8442624 - Ann Intern Med. 1993 Apr 1;118(7):529-39 – reference: 21123811 - Sci Transl Med. 2010 Dec 1;2(60):60rv5 – reference: 18769019 - J Lipid Res. 2009 Jan;50(1):47-58 – reference: 22790967 - Toxicol Sci. 2012 Oct;129(2):456-68 – reference: 18579710 - Mol Pharmacol. 2008 Sep;74(3):662-72 – reference: 22438574 - Diabetes. 2012 Jun;61(6):1543-51 – reference: 5784786 - N Engl J Med. 1969 Jul 10;281(2):91-2 – reference: 15340055 - Mol Cell Biol. 2004 Sep;24(18):7931-40 – reference: 22609277 - Trends Pharmacol Sci. 2012 Jun;33(6):323-30 – reference: 21295138 - Biochim Biophys Acta. 2011 Aug;1812(8):956-63 – reference: 21897230 - Curr Opin Lipidol. 2011 Dec;22(6):460-6 |
SSID | ssj0006060 |
Score | 2.4514954 |
Snippet | The pregnane X receptor (PXR), along with its sister receptor constitutive androstane receptor (CAR), was initially characterized as a xenobiotic receptor that... |
SourceID | pubmedcentral proquest gale pubmed pascalfrancis crossref |
SourceType | Open Access Repository Aggregation Database Index Database Enrichment Source |
StartPage | 1876 |
SubjectTerms | Ablation Adipocytes Analysis Animals Biological and medical sciences Blotting, Western Body composition Calorimetry Cellular proteins Diabetes Diabetes. Impaired glucose tolerance Diet Diet, High-Fat - adverse effects Endocrine pancreas. Apud cells (diseases) Endocrinopathies Enzymes Etiopathogenesis. Screening. Investigations. Target tissue resistance Fatty acids Glucose Glucose Tolerance Test Homeostasis Hyperglycemia Insulin resistance Insulin Resistance - genetics Insulin Resistance - physiology Kinases Medical sciences Metabolic diseases Metabolism Mice Obesity Obesity - etiology Obesity - genetics Obesity - surgery Original Research Oxidation Physiological aspects Receptors, Steroid - genetics Receptors, Steroid - metabolism |
Title | PXR Ablation Alleviates Diet-Induced and Genetic Obesity and Insulin Resistance in Mice |
URI | https://www.ncbi.nlm.nih.gov/pubmed/23349477 https://www.proquest.com/docview/1426056951 https://www.proquest.com/docview/1355480011 https://pubmed.ncbi.nlm.nih.gov/PMC3661619 |
Volume | 62 |
hasFullText | 1 |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV3fb9MwELZgkxASQvwmMCqD0ODFWmIntveEStkYiI6pYqJvVuw4Y9KUFtL-_9zFbragipdKsa9OfL7Y3znn7wh562HJrZS0zOe5ZbkoFbNWKAaLRVppXWnR0S5OT-XJef51Xszjhlsbwyo3c2I3UVcLh3vkBxlSqRcSAMGH5W-GWaPw62pMoXGb7CJ1GVq1mvcOVwrgPBxByTjScKrALMTh9geVxbIUc4TfWI_irHxvWbagoTqkttiGPf8NobyxJh0_IPcjmKTjMPoPyS3fPCJ3pvFz-WPy82w-o2Mbwt3o-AqPkiO2pJ8u_Yph1g7nK1o2FUX2aWiExjwBXdmXEKZOZ1CEGNJ5CldTmFmekPPjox-TExYzKTAnlVwxX-aWO-4AnNaVT11dFxjbminpC2F1WWXg5eVOcNCKV05rm4NnWJRc2tJVXIqnZKdZNP45od7LvBaqFhqZ250ua80F3MWn9hBGPU_I-40-jYs045jt4sqAu4GqN6h6g6pPyJtedBm4NbYJ7eOgGOSqaDAYxoUNFQP9m3w3YwH4sygAlkJrQ8GLct22Rn_-NhB6F4XqBTyVK-MhBOgb8mANJPcHkheBBXyb4N5AEF5PN6geDayp7ylXOaDdQwn_35iXifNHa66tPSGv-2psGmPiGr9YgwxCRY2YPiHPgjVeNy6QdkiphKiBnfYCyCo-rGkuf3Xs4gIQG3jVL_7_WC_JXR4Sg7A02yM7qz9r_wrg2cqOuncQfvUkG5Hdj0enZ7O_JnA5cA |
linkProvider | ProQuest |
linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1db9MwFLXGkGASQnyOwBgGwcZLtMR2Yu8BoapjtKwdaNpE30zsOGPSlBbSCvGn-I3cG6ftgire9ljnxI3ta_vc5PpcQl472HJzmZrQCWFCwTMZGsNlCJtFlCuVK17LLg6P096Z-DRKRmvkz_wsDIZVztfEeqHOxxbfke_FKKWepEAI3k9-hJg1Cr-uzlNoeLM4cr9_gctWvesfwPi-Yezww2m3FzZZBUKbynQaukwYZpkFolbkLrJFkWCcZyxTl3CjsjwGj0dYzkzMnLRKGQFeUpKx1GQ2ZymHem-QmwIagTNKdZchJeAM-CMvMUPZT-mVjBgg93KDZRHmJL-y_zW7wJ1JVsGIFD6Vxiqu-2_I5pU98PAeuduQV9rx1nafrLnyAbk1bD7PPyRfv4xOaMf48DraucSj68hl6cGFm4aYJcS6nGZlTlHtGiqhTV6Cuqzvw-LpCRQhZ7WOwq8hrGSPyNm19PFjsl6OS_eEUOdSUXBZcIVK8VZlhWIc_sVFZh-sTATk7bw_tW1kzTG7xqUG9wa7XmPXa-z6gLxaQCdey2MVaAcHRaM2RonBN9a_wNHQvu5n3eHAd5MEaDDU1gaeZ7Oq0urjoAXabUDFGJ7KZs2hB2gb6m61kDst5LlXHV8F3GoBYTmwrcvbLWtatJRJAex6P4X75-alm_Wq0svZFZCXi8tYNcbglW48AwxSU4U-REA2vTUuK-cocyRlQGTLThcAVDFvXykvvtdq5hwYInjxT___WC_I7d7pcKAH_eOjZ2SD-aQkYRRvkfXpz5l7DtRwarbr-UjJt-teAP4C8Px0Lg |
linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1db9MwFLXGkCYkhPgmMIZBMHiJmthJ7D0gVLWUla1jmpjWN2M7zpg0pYW0Qvw1fh33xmm7oIq3PdY5cWP72j43uT6XkNcOttxcZCZ0SWLChGsRGsNFCJtFlEuZS17LLo6Osv3T5PM4HW-QP4uzMBhWuVgT64U6n1h8R96JUUo9zYAQdIomLOK4P_gw_RFiBin80rpIp-FN5MD9_gXuW_V-2IexfsPY4OPX3n7YZBgIbSayWeh0YphlFkhbkbvIFkWKMZ-xyFzKjdR5DN5PYjkzMXPCSmkS8JhSzTKjbc4yDvXeIDcFFxLnmOytwkvAMfDHX2KGEqDCqxoxaHonN1gWYX7yK3thsyPcnuoKRqfwaTXW8d5_wzev7IeDu-ROQ2Rp11vePbLhyvtka9R8qn9Azo7HJ7RrfKgd7V7iMXbktbR_4WYhZgyxLqe6zCkqX0MltMlRUJcNfYg8PYEi5K_WUfg1glXtITm9lj5-RDbLSemeEOpclhRcFFyiaryVupCMw7-4yOyBxSUBebfoT2UbiXPMtHGpwNXBrlfY9Qq7PiCvltCp1_VYB9rFQVGok1GixVn_MkdB-3pfVJcD901ToMRQWxt4rudVpeSnwxbobQMqJvBUVjcHIKBtqMHVQu62kOdegXwdcLsFhKXBti7vtKxp2VImEmDaexncvzAv1axdlVrNtIC8XF7GqjEer3STOWCQpkr0JwLy2FvjqnKOkkdCBES07HQJQEXz9pXy4nutbM6BLYJH__T_j_WCbMHUV4fDo4Nn5Bbz-UnCKN4mm7Ofc_ccWOLM7NTTkZJv1z3__wJ093hk |
openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=PXR+ablation+alleviates+diet%2C+induced+and+genetic+obesity+and+insulin+resistance+in+mice&rft.jtitle=Diabetes+%28New+York%2C+N.Y.%29&rft.au=He%2C+Jinhan&rft.au=Gao%2C+Jie&rft.au=Xu%2C+Meishu&rft.au=Ren%2C+Songrong&rft.date=2013-06-01&rft.pub=American+Diabetes+Association&rft.issn=0012-1797&rft.volume=62&rft.issue=6&rft.spage=1876&rft_id=info:doi/10.2337%2Fdb12-1039&rft.externalDocID=A332655565 |
thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0012-1797&client=summon |
thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0012-1797&client=summon |
thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0012-1797&client=summon |