Search results for "Cholesterol 7 alpha-hydroxylase"

showing 10 items of 14 documents

Nonacidic Farnesoid X Receptor Modulators.

2017

As a cellular bile acid sensor, farnesoid X receptor (FXR) participates in regulation of bile acid, lipid and glucose homeostasis, and liver protection. Clinical results have validated FXR as therapeutic target in hepatic and metabolic diseases. To date, potent FXR agonists share a negatively ionizable function that might compromise their pharmacokinetic distribution and behavior. Here we report the development and characterization of a high-affinity FXR modulator not comprising an acidic residue.

0301 basic medicineMalemedicine.drug_classPyridinesPeroxisome proliferator-activated receptorReceptors Cytoplasmic and NuclearATP-binding cassette transporterCholesterol 7 alpha-hydroxylase01 natural sciencesRats Sprague-Dawley03 medical and health sciencesStructure-Activity RelationshipDrug StabilityDrug DiscoverymedicineGlucose homeostasisAnimalsHumansPPAR alphaReceptorCholesterol 7-alpha-HydroxylaseATP Binding Cassette Transporter Subfamily B Member 11chemistry.chemical_classificationBile acid010405 organic chemistryChemistryHEK 293 cellsImidazolesMembrane Transport ProteinsHep G2 Cells0104 chemical sciencesMolecular Docking SimulationZolpidem030104 developmental biologyHEK293 CellsBiochemistryMolecular MedicineFarnesoid X receptorATP-Binding Cassette TransportersSterol Regulatory Element Binding Protein 1HeLa CellsJournal of medicinal chemistry
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Infant Formula Feeding Increases Hepatic Cholesterol 7α Hydroxylase (CYP7A1) Expression and Fecal Bile Acid Loss in Neonatal Piglets.

2018

BACKGROUND: During the postnatal feeding period, formula-fed infants have higher cholesterol synthesis rates and lower circulating cholesterol concentrations than their breastfed counterparts. Although this disparity has been attributed to the uniformly low dietary cholesterol content of typical infant formulas, little is known of the underlying mechanisms associated with this altered cholesterol metabolism phenotype. OBJECTIVE: We aimed to determine the molecular etiology of diet-associated changes in early-life cholesterol metabolism with the use of a postnatal piglet feeding model. METHODS: Two-day-old male and female White-Dutch Landrace piglets were fed either sow milk (Sow group) or d…

0301 basic medicineMalemedicine.medical_specialtymedicine.drug_classSwineMedicine (miscellaneous)030209 endocrinology & metabolismCholesterol 7 alpha-hydroxylaseReal-Time Polymerase Chain ReactionGene Expression Regulation EnzymologicBile Acids and Salts03 medical and health scienceschemistry.chemical_compoundFecesRandom Allocation0302 clinical medicineBlood serumInternal medicinemedicineAnimalsHumansCholesterol 7-alpha-HydroxylaseEnterohepatic circulationNutrition and DieteticsBile acidCholesterolReverse Transcriptase Polymerase Chain ReactionInfantFGF19Infant Formula030104 developmental biologyEndocrinologyMilkchemistryInfant formulaAnimals NewbornLiverFemaleSoybeansNutrient Physiology Metabolism and Nutrient-Nutrient InteractionsBreast feedingThe Journal of nutrition
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Gene-diet interaction in plasma lipid response to plant sterols and stanols: A review of clinical trials

2021

Abstract Plant sterols and stanols (PS) are well known for their cholesterol-lowering effect by reducing intestinal absorption of cholesterol. However, genetic factors modulate the low-density lipoprotein cholesterol (LDL-C) response to PS therapy. This review examines clinical trials evaluating the impact of the main genes associated with response of plasma lipid concentrations to PS intake: APOE, CYP7A1, ABCG5/G8, NPC1L1, CETP, APOA4/A5, SCARBI, HMGCR, PPARα, LIPC, MTHFR and LPA. Evidence indicates that carriers of mutant allele of the CYP7A1 c. −204 A > C variant experience a greater plasma cholesterol reduction after PS intake, although there is discrepancy for the rest of genetic varia…

Apolipoprotein Emedicine.medical_specialtyLipid-lowering effectMedicine (miscellaneous)Cholesterol 7 alpha-hydroxylaseInterindividual variabilityIntestinal absorptionchemistry.chemical_compoundAPOA4Internal medicinemedicineTX341-641NutrigeneticsGen-dietNutrition and DieteticsbiologyNutrition. Foods and food supplyCholesterolbusiness.industryPlant sterols/stanolsClinical trialEndocrinologychemistryMethylenetetrahydrofolate reductaseABCG5biology.proteinlipids (amino acids peptides and proteins)businessFood ScienceJournal of Functional Foods
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CLA-Enriched Diet Containing t10,c12-CLA Alters Bile Acid Homeostasis and Increases the Risk of Cholelithiasis in Mice

2011

International audience; Mice fed a mixture of CLA containing t10,c12-CLA lose fat mass and develop hyperinsulinemia and hepatic steatosis due to an accumulation of TG and cholesterol. Because cholesterol is the precursor in bile acid (BA) synthesis, we investigated whether t10,c12-CLA alters BA metabolism. In Expt. 1, female C57Bl/6J mice were fed a standard diet for 28 d supplemented with a CLA mixture (1 g/100 g) or not (controls). In Expt. 2, the feeding period was reduced to 4, 6, and 10 d. In Expt. 3, mice were fed a diet supplemented with linoleic acid, c9,t11-CLA, or t10,c12-CLA (0.4 g/100 g) for 28 d. In Expt. 1, the BA pool size was greater in CLA-fed mice than in controls and the …

Enterohepatic circulationmedicine.medical_specialtymedicine.drug_classLinoleic acid[SDV]Life Sciences [q-bio]Blotting WesternMedicine (miscellaneous)030209 endocrinology & metabolismCholesterol 7 alpha-hydroxylasePolymerase Chain ReactionBile Acids and SaltsMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRisk FactorsCholelithiasisInternal medicineHyperinsulinémiemedicineHyperinsulinemiaAnimalsHomeostasisEnterohepatic circulation030304 developmental biology0303 health sciencesNutrition and DieteticsBile acidintegumentary systemCholesterolalpha-Linolenic Acidfood and beveragesmedicine.diseaseDietary FatsBile Salt Export PumpMice Inbred C57BLCholesterol 7-alpha hydroxylaseCholesterolEndocrinologyMetabolismLiverchemistryNutrient physiologyFemalelipids (amino acids peptides and proteins)Steatosis[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition
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Mobilization of late-endosomal cholesterol is inhibited by Rab guanine nucleotide dissociation inhibitor

2000

AbstractCholesterol entering cells in low-density lipoproteins (LDL) via receptor-mediated endocytosis is transported to organelles of the late endocytic pathway for degradation of the lipoprotein particles. The fate of the free cholesterol released remains poorly understood, however. Recent observations suggest that late-endosomal cholesterol sequestration is regulated by the dynamics of lysobisphosphatidic acid (LBPA)-rich membranes [1]. Genetic studies have pinpointed a protein, Niemann–Pick C-1 (NPC-1), that is required for the mobilization of late-endosomal/lysosomal cholesterol by an unknown mechanism [2]. Here, we report the removal of accumulated cholesterol by overexpression of the…

HydrolasesEndosomeEndocytic cycleEndosomesCholesterol 7 alpha-hydroxylaseGeneral Biochemistry Genetics and Molecular BiologyCell Line03 medical and health scienceschemistry.chemical_compound0302 clinical medicineHumansGuanine Nucleotide Dissociation Inhibitors030304 developmental biologyNiemann-Pick Diseases0303 health sciencesbiologyAgricultural and Biological Sciences(all)CholesterolBiochemistry Genetics and Molecular Biology(all)Reverse cholesterol transportCholesterol LDLEndocytosisRecombinant ProteinsCell biologyCholesterolchemistryBiochemistryHMG-CoA reductasebiology.proteinMonoglycerideslipids (amino acids peptides and proteins)RabLysophospholipidsLysosomesGeneral Agricultural and Biological Sciences030217 neurology & neurosurgeryLipoproteinCurrent Biology
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NPC1L1 and ABCG5/8 induction explain synergistic fecal cholesterol excretion in ob/ob mice co-treated with PPAR-α and LXR agonists

2020

Reverse cholesterol transport (RCT) and transintestinal cholesterol efflux (TICE) are two important pathways for body cholesterol elimination. We studied these pathways in an animal model of diabetes and obesity (ob/ob) where HDL function is compromised as a result of hyperglycemia, low-grade inflammation and oxidative stress. Co-treatment of ob/ob mice with PPAR-α (fenofibrate) and LXR (T0901317) agonists increased fecal cholesterol by 12-fold; PPAR-α and LXR agonists individually showed 2.6- and 4.0-fold fecal cholesterol excretion, respectively. We investigated the mechanism of synergistic efficacy of PPAR-α and LXR agonists in fecal cholesterol excretion. LXR agonist and the combination…

Male0301 basic medicinemedicine.medical_specialtyHydrocarbons FluorinatedHDLLipoproteinsClinical BiochemistryMice ObeseABCA1NPC1L1Cholesterol 7 alpha-hydroxylaseExcretionFecesMiceob/ob03 medical and health scienceschemistry.chemical_compound0302 clinical medicineFenofibrateInternal medicinemedicineAnimalsPPAR alphaTICEATP Binding Cassette Transporter Subfamily G Member 5Liver X receptorMolecular BiologyLiver X ReceptorsSulfonamidesFenofibratebiologyChemistryCholesterolATP Binding Cassette Transporter Subfamily G Member 8Reverse cholesterol transportMembrane Transport ProteinsDrug SynergismCell BiologyGeneral MedicineCholesterol030104 developmental biologyEndocrinology030220 oncology & carcinogenesisABCA1ABCG5/G8biology.proteinIntestinal cholesterol absorptionlipids (amino acids peptides and proteins)medicine.drugMolecular and Cellular Biochemistry
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Cyclosporine A Impairs the Macrophage Reverse Cholesterol Transport in Mice by Reducing Sterol Fecal Excretion

2012

Despite the efficacy in reducing acute rejection events in organ transplanted subjects, long term therapy with cyclosporine A is associated with increased atherosclerotic cardiovascular morbidity. We studied whether this drug affects the antiatherogenic process of the reverse cholesterol transport from macrophages in vivo. Cyclosporine A 50 mg/kg/d was administered to C57BL/6 mice by subcutaneous injection for 14 days. Macrophage reverse cholesterol transport was assessed by following [(3)H]-cholesterol mobilization from pre-labeled intraperitoneally injected macrophages, expressing or not apolipoprotein E, to plasma, liver and feces. The pharmacological treatment significantly reduced the …

MaleApolipoprotein EMouselcsh:MedicineCardiovascularBiochemistryFecesMiceSubcutaneous injectionchemistry.chemical_compoundIntestinal Mucosalcsh:ScienceCholesterol 7-alpha-HydroxylaseMultidisciplinaryReverse cholesterol transportAnimal ModelsLipidsIntestinesCholesterolLiverCyclosporineMedicinelipids (amino acids peptides and proteins)Research Articlemedicine.medical_specialtyLipoproteinsTritiumCholesterol 7 alpha-hydroxylaseCardiovascular PharmacologyExcretionApolipoproteins EModel OrganismsIn vivoInternal medicinemedicineAnimalsBiologyCholesterollcsh:RProteinsBiological TransportLipid MetabolismAtherosclerosisSitosterolsSterolMice Inbred C57BLKineticsEndocrinologyGene Expression RegulationchemistryMacrophages Peritoneallcsh:QATP-Binding Cassette TransportersPLoS ONE
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Intestinal cholesterol absorption: identification of different binding proteins for cholesterol and cholesterol absorption inhibitors in the enterocy…

2003

Absorption of cholesterol from the intestine is a central part of body cholesterol homeostasis. The molecular mechanisms of intestinal cholesterol absorption and the proteins mediating membrane transport are not known. We therefore aimed to identify the proteins involved in intestinal cholesterol absorption across the luminal brush border membrane of small intestinal enterocytes. By photoaffinity labeling using photoreactive derivatives of cholesterol and 2-azetidinone cholesterol absorption inhibitors, an 80-kDa and a 145-kDa integral membrane protein were identified as specific binding proteins for cholesterol and cholesterol absorption inhibitors, respectively, in the brush border membra…

MaleBrush bordermedicine.drug_classBiologyCholesterol 7 alpha-hydroxylaseIntestinal absorptionSubstrate SpecificityCholesterol DietaryEzetimibeIntestine SmallmedicineAnimalsTissue DistributionCholesterol absorption inhibitorMolecular BiologyMicrovilliMolecular StructureAnticholesteremic AgentsReverse cholesterol transportMembrane ProteinsBiological TransportCell BiologyMembrane transportMolecular WeightEnterocytesIntestinal AbsorptionBiochemistryIntestinal cholesterol absorptionlipids (amino acids peptides and proteins)RabbitsCarrier Proteinsmedicine.drugBiochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids
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Effects of peroxisome proliferator-activated receptor alpha activation on pathways contributing to cholesterol homeostasis in rat hepatocytes

2004

International audience; Peroxisome proliferator-activated receptor alpha (PPARa) activation by fibrates controls expression of several genes involved in hepatic cholesterol metabolism. Other genes could be indirectly controlled in response to changes in cellular cholesterol availability. To further understand how fibrates may affect cholesterol synthesis, we investigated in parallel the changes in the metabolic pathways contributing to cholesterol homeostasis in liver. Ciprofibrate increased HMG-CoA reductase and FPP synthase mRNA levels in rat hepatocytes, together with cholesterogenesis from [14C] acetate and [3H] mevalonate. The up-regulation observed in fenofibrate- and WY-14,643-treate…

MaleCarboxy-Lyases[SDV]Life Sciences [q-bio]Receptors Cytoplasmic and NuclearAcetatesClofibric AcidMicechemistry.chemical_compound0302 clinical medicineMice KnockoutCarbon Isotopes0303 health sciencesFenofibrateFibric AcidsPeroxisomeUp-RegulationHMG-COA REDUCTASEDNA-Binding ProteinsCholesterolCHOLESTEROL METABOLISM030220 oncology & carcinogenesisHMG-CoA reductaseCholesteryl esterPeroxisome Proliferatorslipids (amino acids peptides and proteins)Peroxisome proliferator-activated receptor alphaSterol Regulatory Element Binding Protein 1Cell DivisionSignal Transductionmedicine.drugmedicine.medical_specialtyMevalonic AcidPeroxisome ProliferationBiologyCholesterol 7 alpha-hydroxylaseBile Acids and Salts03 medical and health sciencesInternal medicinemedicineAnimalsRNA MessengerMolecular Biology030304 developmental biologyCell BiologyRAT HEPATOCYTEPPARA-NULL MOUSERatsSterol regulatory element-binding proteinMice Inbred C57BLPyrimidinesEndocrinologychemistryFIBRATECCAAT-Enhancer-Binding ProteinsHepatocytesbiology.proteinHydroxymethylglutaryl CoA ReductasesTranscription Factors
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Molecular mechanisms of hepatotoxic cholestasis by clavulanic acid: Role of NRF2 and FXR pathways.

2021

Treatment of β-lactamase positive bacterial infections with a combination of amoxicillin (AMOX) and clavulanic acid (CLAV) causes idiosyncratic drug-induced liver injury (iDILI) in a relevant number of patients, often with features of intrahepatic cholestasis. This study aims to determine serum bile acid (BA) levels in amoxicillin/clavulanate (A + C)-iDILI patients and to investigate the mechanism of cholestasis by A + C in human in vitro hepatic models. In six A + C-iDILI patients, significant elevations of serum primary conjugated BA definitely demonstrated A + C-induced cholestasis. In cultured human Upcyte hepatocytes and HepG2 cells, CLAV was more cytotoxic than AMOX, and, at subcytoto…

Malemedicine.drug_classNF-E2-Related Factor 2Receptors Cytoplasmic and NuclearCholestasis IntrahepaticPharmacologyToxicologyCholesterol 7 alpha-hydroxylaseCell Linechemistry.chemical_compoundDownregulation and upregulationCholestasismedicineHumansClavulanic AcidAgedLiver injuryBile acidChemistryGeneral MedicineGlutathioneMiddle Agedmedicine.diseaseFarnesoid X receptorFemaleCYP8B1Food ScienceSignal TransductionFood and chemical toxicology : an international journal published for the British Industrial Biological Research Association
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