Search results for "Estradiol"

showing 10 items of 203 documents

Aromatase Inhibitors Plus Weight Loss Improves the Hormonal Profile of Obese Hypogonadal Men Without Causing Major Side Effects

2020

Objective: In obese men, the increased expression of the aromatase enzyme in adipose tissue leads to high conversion of androgens to estrogens contributing to hypogonadotropic hypogonadism (HHG). Our objective is to evaluate efficacy and safety of weight loss (WL) plus aromatase inhibitor (AI) therapy in severely obese men with HHG. We hypothesize that AI+WL will be more effective as compared to WL alone in improving the hormonal profile, thus muscle strength and symptoms of HHG (primary outcomes), with no significant adverse effects on lean mass, metabolic profile, and bone mineral density (secondary outcomes).Design: Randomized double-blind placebo-controlled pilot trial.Methods: Twenty-t…

Male0301 basic medicineobesityBone densityEndocrinology Diabetes and MetabolismPilot Projectslcsh:Diseases of the endocrine glands. Clinical endocrinologyaromatase inhibitorsEndocrinology0302 clinical medicineBone DensityWeight lossMedicineTestosteroneTestosteroneBone mineralEstradiolMiddle AgedPrognosisClinical TrialAndrogensMetabolomemedicine.symptombone microarchitecturemedicine.drugAdultmedicine.medical_specialtyHormone Replacement Therapymedicine.drug_classAnastrozole030209 endocrinology & metabolismsex hormonesBone and Bones03 medical and health sciencesDouble-Blind MethodHypogonadotropic hypogonadismInternal medicineWeight LossHumanshypogonadismMuscle StrengthAgedbody compositionlcsh:RC648-665Aromatase inhibitorbusiness.industrymedicine.disease030104 developmental biologyEndocrinologyLean body massbusinessBiomarkersFollow-Up StudiesFrontiers in Endocrinology
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Post-transcriptional analysis of rat mitochondrial D-3-hydroxybutyrate dehydrogenase control through development and physiological stages.

1991

Abstract The nuclear encoded mitochondrial D -3-hydroxybutyrate dehydrogenase (BDH) is synthesized in the cytosal as a larger precursor. This membrane enzyme which requires lecithin for activity plays an essential role in energy metabolism as a ketone bodies-converting enzyme. A cDNA clone of the rat liver enzyme encompassing an antigenic determinant peptide has been isolated after immunoscreening of a λ gt11 expression library. The nucleotide sequence of this 279-base cDNA insert contains a single open reading frame of 93 amino-acids, which represents about a third of the mature enzyme. Amino-acid sequence analysis predicts a hydrophobic stretch of 29 amino-acids long which probably functi…

MaleAgingBlotting WesternMolecular Sequence DataBiologyGene Expression Regulation EnzymologicEnzyme activatorHydroxybutyrate DehydrogenaseComplementary DNAImmunoscreeningGene expressionAnimalsAmino Acid SequenceCloning MolecularRNA Processing Post-TranscriptionalGenechemistry.chemical_classificationMessenger RNASex CharacteristicsBase SequenceEstradiolRats Inbred StrainsCell BiologyGeneral MedicineDNABlotting NorthernEmbryo MammalianMolecular biologyDietary FatsMitochondriaRatsOpen reading frameEnzymeBiochemistrychemistryOrgan SpecificityFemaleCorticosteroneBiology of the cell
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Direct antioxidant and protective effect of estradiol on isolated mitochondria

2009

AbstractEstrogens have antioxidant properties which are due to their ability to bind to estrogen receptors and to up-regulate the expression of antioxidant enzymes via intracellular signalling pathways. Mitochondria are key organelles in the development of age-associated cellular damage. Recently, estrogen receptors were identified in mitochondria. The aim of this paper was to test whether estradiol directly affects mitochondria by preventing oxidative stress and protecting frail mitochondria. Incubation with estradiol at normal intracellular concentrations prevents the formation of reactive oxygen species by mitochondria in a saturable manner. Moreover, estradiol protects mitochondrial int…

MaleAgingCytochromeCytochrome cGenisteinMitochondrionmedicine.disease_causeAntioxidantschemistry.chemical_compoundmedicineAnimalsRats WistarMolecular BiologyCells Culturedchemistry.chemical_classificationReactive oxygen speciesbiologyDose-Response Relationship DrugEstradiolCytochrome cCytochromes cEstrogenic compoundGenisteinMitochondriaRatsOxidative StressBiochemistrychemistryApoptosisbiology.proteinMolecular MedicineApoptosomeAntioxidantReactive Oxygen Specieshormones hormone substitutes and hormone antagonistsOxidative stressBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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Differential regulation by a peroxisome proliferator of the different multifunctional proteins in guinea pig: cDNA cloning of the guinea pig D-specif…

1998

After our previous report on the cloning of two cDNA species in guinea pig, both encoding the same hepatic 79 kDa multifunctional protein 1 (MFP-1) [Caira, Cherkaoui-Malki, Hoefler and Latruffe (1996) FEBS Lett. 378, 57-60], here we report the cloning of a cDNA encoding a second multifunctional peroxisomal protein (MFP-2) in guinea-pig liver. This 2356 nt cDNA encodes a protein of 735 residues (79.7 kDa) whose sequence shows 83% identity with rat MFP-2 [Dieuaide-Noubhani, Novikov, Baumgart, Vanhooren, Fransen, Goethals, Vandekerckhove, Van Veldhoven and Mannaerts (1996) Eur. J. Biochem. 240, 660-666]. In parallel, we studied the effect of ciprofibrate, a hypolipaemic agent also known as per…

MaleDNA ComplementaryTranscription GeneticGuinea PigsMolecular Sequence DataBiologyMicrobodiesBiochemistryEstradiol DehydrogenasesRats Sprague-DawleyGuinea pigClofibric AcidComplementary DNAGene expressionmedicineAnimalsAmino Acid SequenceRNA MessengerNorthern blotCloning MolecularEnoyl-CoA HydrataseMolecular BiologyHypolipidemic AgentsMessenger RNABase SequenceThiolaseFibric AcidsCell BiologyPeroxisomeMolecular biologyRatsGene Expression RegulationLiverBiochemistryCiprofibrateOxidoreductasesResearch Articlemedicine.drugBiochemical Journal
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Prevalence and clinical features of polycystic ovarian syndrome in adolescents with previous childhood growth hormone deficiency.

2016

AbstractGrowth hormone (GH) plays a role in the regulation of ovarian function but there are limited data in women with GH deficiency (GHD). Our aim was to evaluate the features of polycystic ovarian syndrome (PCOS) in women with previous GHD.Data of 22 adolescents previously GH-treated (group A) were compared with those of 22 women with classical PCOS (group B) and 20 controls (group C).: Group A showed higher testosterone (p=0.048) and prevalence of menstrual irregularities (p<0.001) than group C. Compared to the group B, group A showed lower diastolic blood pressure (p=0.004), degree of hirsutism (p=0.005), testosterone (p=0.003) and prevalence of polycsytic ovaries (POC) morphology (…

MaleHirsutismmedicine.medical_specialtyAdolescentChildhood growthEndocrinology Diabetes and Metabolism030209 endocrinology & metabolismGroup AGroup BSettore MED/13 - Endocrinologia03 medical and health sciences0302 clinical medicineEndocrinologyInternal medicinePrevalenceHumansMedicineTestosteroneProspective StudiesChildGrowth DisordersMenstruation DisturbancesTestosteronehirsutism030219 obstetrics & reproductive medicineEstradiolHuman Growth Hormonebusiness.industryPrognosismedicine.diseaseGrowth hormone polycystic ovarian syndromeEndocrinologyBlood pressureItalyCase-Control StudiesPediatrics Perinatology and Child HealthFemaleHyperandrogenismbusinessBiomarkersGH DeficiencyFollow-Up StudiesPolycystic Ovary SyndromeHormone
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Part of the Series: From Dietary Antioxidants to Regulators in Cellular Signalling and Gene ExpressionRole of reactive oxygen species and (phyto)oest…

2006

There is increasing evidence that reactive oxygen species (ROS) are not only toxic but play an important role in cellular signalling and in the regulation of gene expression. We, here, discuss two examples of improved adaptive response to an altered cellular redox state. First, differences in longevity between males and females may be explained by a higher expression of antioxidant enzymes in females resulting in a lower yield of mitochondrial ROS. Oestrogens are made responsible for these phenomena. Oestradiol induces glutathione peroxidase-1 and MnSOD by processes requiring the cell surface oestrogen receptor (ER) and the activation of pathways usually involved in oxidative stress respons…

MaleMitochondrial ROSAgingAntioxidantmedicine.medical_treatmentGene ExpressionPhytoestrogensmedicine.disease_causeBiochemistryAntioxidantsSuperoxide dismutasechemistry.chemical_compoundGlutathione Peroxidase GPX1medicineAnimalsHumansRegulation of gene expressionchemistry.chemical_classificationGlutathione PeroxidaseReactive oxygen speciesEstradiolbiologySuperoxide DismutaseGeneral MedicineGlutathioneCatalaseRatsOxidative StressReceptors EstrogenBiochemistrychemistryCatalaseDietary Supplementsbiology.proteinFemaleReactive Oxygen SpeciesOxidation-ReductionOxidative stressSignal TransductionFree Radical Research
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Estrogens inhibit angiotensin II-induced leukocyte-endothelial cell interactions in vivo via rapid endothelial nitric oxide synthase and cyclooxygena…

2002

Angiotensin II (Ang II) may be a key molecule in the development of atherosclerosis. Because the incidence of coronary atherosclerosis in premenopausal women is lower than that observed in men or postmenopausal women, we have investigated the effect of estrogens on Ang II–induced leukocyte recruitment in vivo using intravital microscopy in the rat mesenteric microcirculation. Superfusion for 60 minutes with Ang II induced a significant increase in leukocyte rolling flux, adhesion, and emigration. Administration of 17-β-estradiol (17-β-E) after 30 minutes of Ang II superfusion produced a reduction of these leukocyte responses by 55.1%, 72.7%, and 70.9%, respectively, an additional 30 minutes…

MaleSelective Estrogen Receptor Modulatorsmedicine.medical_specialtyEndotheliumPhysiologyLeukocyte RollingProstacyclinCell CommunicationBiologyIn Vitro TechniquesLosartanReceptor Angiotensin Type 1Lymphatic SystemRats Sprague-DawleyAngiotensin Receptor AntagonistsCell MovementInternal medicinemedicineCell AdhesionLeukocytesAnimalsHumansSplanchnic CirculationEnzyme InhibitorsCells CulturedVenuleEstradiolAngiotensin IIEstrogen AntagonistsAntibodies MonoclonalEstrogensAngiotensin IIEpoprostenolRatsEndothelial stem cellNitric oxide synthasemedicine.anatomical_structureEndocrinologyProstaglandin-Endoperoxide Synthasesbiology.proteinEndothelium VascularNitric Oxide SynthaseCardiology and Cardiovascular Medicinehormones hormone substitutes and hormone antagonistsIntravital microscopymedicine.drugCirculation research
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Anti-atherogenic Effects of 17β-Estradiol

2013

Estrogens are secreted primarily by the ovaries and placenta, by the testes in men and also produced by peripheral steroidogenic conversion. The 3 major naturally occurring estrogens are: 17β-estradiol (E2), estrone and estriol, of which E2 is the predominant and most active. The actions of E2 are mediated by at least 3 different receptors - the classical ERs (ERα and ERβ) and G-protein coupled receptor 30 (GPR30). E2 signaling in cardiomyocytes involves ERα- and ERβ-independent pathways, and treatment with the E2 receptor antagonists (Selective Estrogen Receptor Modulators- SERMs), which are agonists of GPR30, inhibits cardiac cell growth. Effects of E2 in preventing endothelial dysfunctio…

MaleSelective Estrogen Receptor Modulatorsmedicine.medical_specialtyVascular smooth muscleEndotheliummedicine.drug_classEndocrinology Diabetes and MetabolismOvariectomyClinical BiochemistryInflammation030204 cardiovascular system & hematologyBiologyBiochemistry03 medical and health sciencesestrogen 17β-estradiol atherogenic factors atherosclerosis0302 clinical medicineEndocrinologyRisk FactorsInternal medicinemedicineAnimalsHumansEndothelial dysfunctionReceptorEstradiolBiochemistry (medical)Estrogen Replacement TherapyGeneral Medicinemedicine.diseaseAtherosclerosis3. Good healthmedicine.anatomical_structureEndocrinologySelective estrogen receptor modulatorEstrogen030220 oncology & carcinogenesisDiet AtherogenicFemalemedicine.symptomGPER
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Estradiol induces endothelial cell migration and proliferation through estrogen receptor-enhanced RhoA/ROCK pathway

2010

Migration and proliferation of endothelial cells are involved in re-endothelialization and angiogenesis, two important cardiovascular processes that are increased in response to estrogens. RhoA, a small GTPase which controls multiple cellular processes, is involved in the control of cell migration and proliferation. Our aim was to study the role of RhoA on estradiol-induced migration and proliferation and its dependence on estrogen receptors activity. Human umbilical vein endothelial cells were stimulated with estradiol, in the presence or absence of ICI 182780 (estrogen receptors antagonist) and Y-27632 (Rho kinase inhibitor). Estradiol increased Rho GEF-1 gene expression and RhoA (gene an…

MaleTranscriptional ActivationRHOAAngiogenesismedicine.drug_classEstrogen receptorCell Cycle ProteinsBiochemistryUmbilical CordEndocrinologyCell MovementmedicineHumansReceptorMolecular BiologyCells CulturedCell ProliferationEnzyme Assaysrho-Associated KinasesEstradiolbiologyChemistryEndothelial CellsCell migrationUp-RegulationCell biologyEndothelial stem cellReceptors EstrogenRho kinase inhibitorEstrogenCancer researchbiology.proteinFemalerhoA GTP-Binding Proteinhormones hormone substitutes and hormone antagonistsSignal TransductionMolecular and Cellular Endocrinology
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2-Methoxyestradiol confers neuroprotection and inhibits a maladaptive HIF-1α response after traumatic brain injury in mice

2014

HIF-1α is pivotal for cellular homeostasis in response to cerebral ischemia. Pharmacological inhibition of HIF-1α may reduce secondary brain damage by targeting post-translational mechanisms associated with its proteasomal degradation and nuclear translocation. This study examined the neuroprotective effects of 2-methoxyestradiol (2ME2), the involved HIF-1α-dependent response, and alternative splicing in exon 14 of HIF-1α (HIF-1α∆Ex14) after traumatic brain injury (TBI) in mice. Intraperitoneal 2ME2 administration 30 min after TBI caused a dose-dependent reduction in secondary brain damage after 24 h. 2ME2 was physiologically tolerated, showed no effects on immune cell brain migration, and …

MaleTraumatic brain injuryBlotting WesternIschemiaCellular homeostasisBrain damagePharmacologyBiologyBiochemistryNeuroprotectionBrain IschemiaMitochondrial ProteinsMiceCellular and Molecular Neurosciencechemistry.chemical_compoundPlasminogen Activator Inhibitor 1medicineAnimalsCell NucleusNeuronsEstradiolTumor Necrosis Factor-alphaAlternative splicingMembrane ProteinsExonsHypoxia-Inducible Factor 1 alpha Subunitmedicine.diseaseImmunohistochemistryUp-RegulationMice Inbred C57BLAlternative SplicingProtein TransportNeuroprotective AgentsGene Expression RegulationchemistryBrain InjuriesPlasminogen activator inhibitor-1Tumor necrosis factor alphamedicine.symptomNeuroscienceInjections IntraperitonealSubcellular FractionsJournal of Neurochemistry
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