Search results for " Thyroid Hormone"

showing 10 items of 19 documents

Homozygous Resistance to Thyroid Hormone β: Can Combined Antithyroid Drug and Triiodothyroacetic Acid Treatment Prevent Cardiac Failure?

2017

Resistance to thyroid hormone β (RTHβ) due to homozygous THRB defects is exceptionally rare, with only five kindreds reported worldwide. Cardiac dysfunction, which can be life-threatening, is recognized in the disorder. Here we describe the clinical, metabolic, ophthalmic, and cardiac findings in a 9-year-old boy harboring a biallelic THRB mutation (R243Q), along with biochemical, physiologic, and cardiac responses to carbimazole and triiodothyroacetic acid (TRIAC) therapy. The patient exhibits recognized features (goiter, nonsuppressed thyroid-stimulating hormone levels, upper respiratory tract infections, hyperactivity, low body mass index) of heterozygous RTHβ, with additional characteri…

0301 basic medicineCardiac function curvemedicine.medical_specialtyendocrine systemGoiterendocrine system diseasesEndocrinology Diabetes and Metabolism030209 endocrinology & metabolismCase ReportsCardiovascularthyroidresistance to thyroid hormonehomozygous THRB mutation03 medical and health sciences0302 clinical medicineClinical ResearchInternal medicinemedicine2.1 Biological and endogenous factorsDecompensation2. Zero hungercardiac thyrotoxicosisbusiness.industryThyroidDilated cardiomyopathymedicine.disease3. Good health030104 developmental biologyEndocrinologymedicine.anatomical_structureCarbimazoleHeart Disease6.1 PharmaceuticalsBasal metabolic ratebusinessHormonemedicine.drug
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Effects of 3,5-diiodo-L-thyronine on the liver of high fat diet fed rats

2016

Experimental studies have highlighted that the administration of 3,5-diiodo-L-thyronine (T2) to rats fed diets rich in lipids induces a decrease of cholesterol and triglycerides plasma levels and body weight (BW) without inducing liver steatosis. On the basis of these observations we carried out some experimental <em>in vivo</em> studies to assess the effects of multiple high doses of T2 on the pituitary thyroid axis of rats fed diet rich in lipids. Fifteen male Wistar rats were divided into three groups of five animals each. The first group (N group) received standard diet, the second group was fed with a high fat diet (HFD group), while the third group (HFDT2 group) was additi…

0301 basic medicineHepatic steatosismedicine.medical_specialtyPlant ScienceAdrenocorticotropic hormoneHepatic steatosi010501 environmental sciencesBiologySettore BIO/09 - Fisiologia01 natural sciencesGeneral Biochemistry Genetics and Molecular BiologyPituitary thyroid axis03 medical and health scienceschemistry.chemical_compoundInternal medicinemedicinelcsh:QH301-705.50105 earth and related environmental sciences35-diiodo-L-thyronine; TSH; Thyroid hormone; Hepatic steatosisBiochemistry Genetics and Molecular Biology (all)TriiodothyronineTSHCholesterolBiochemistry (medical)medicine.diseaseSettore CHIM/08 - Chimica Farmaceutica35-diiodo-L-thyronineThyroid hormone030104 developmental biologyEndocrinologylcsh:Biology (General)chemistryThyronineSettore BIO/14 - FarmacologiaAlkaline phosphataseSteatosisHormoneJournal of Biological Research - Bollettino della Società Italiana di Biologia Sperimentale
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Genomic and non-genomic mechanisms of action of thyroid hormones and their catabolite 3,5-diiodo-l-thyronine in Mammals

2020

Since the realization that the cellular homologs of a gene found in the retrovirus that contributes to erythroblastosis in birds (v-erbA), i.e. the proto-oncogene c-erbA encodes the nuclear receptors for thyroid hormones (THs), most of the interest for THs focalized on their ability to control gene transcription. It was found, indeed, that, by regulating gene expression in many tissues, these hormones could mediate critical events both in development and in adult organisms. Among their effects, much attention was given to their ability to increase energy expenditure, and they were early proposed as anti-obesity drugs. However, their clinical use has been strongly challenged by the concomita…

0301 basic medicinenonalcoholic fatty liver diseaseobesityDiiodothyroninesEndogenyReviewthyroid hormone metabolism and transportMitochondrionmedicine.disease_causeProto-Oncogene Maslcsh:Chemistry0302 clinical medicineTranscription (biology)Settore BIO/10 - BiochimicaGene expressionSettore BIO/06 - Anatomia Comparata E CitologiaSettore MED/49 - Scienze Tecniche Dietetiche Applicatelcsh:QH301-705.5SpectroscopyMammalsReceptors Thyroid Hormonehepatic steatosisthyroid hormone mechanisms of actionGeneral Medicineresistance to thyroid hormones (RTH)Computer Science ApplicationsCell biology35-diiodo-L-thyronineThyroid Hormones030209 endocrinology & metabolismBiologyIodide PeroxidaseCatalysisInorganic Chemistry03 medical and health sciencesmedicineAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologyGeneOrganic ChemistryBiological TransportLipid Metabolismhepatic steatosi030104 developmental biologyNuclear receptorlcsh:Biology (General)lcsh:QD1-999MutationBasal MetabolismLipid PeroxidationOxidative stressHormone
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RORgamma-expressing Th17 cells induce murine chronic intestinal inflammation via redundant effects of IL-17A and IL-17F.

2008

Background and Aims IL-17–producing CD4 + T-helper cells (Th17) contribute to chronic autoimmune inflammation in the brain, and levels of Th17-derived cytokines increase in patients with colitis, suggesting a role in pathogenesis. We analyzed the roles of Th17 cells and the transcription factor retinoic acid receptor-related organ receptor (ROR)γ, which regulates Th17 differentiation, in chronic intestinal inflammation. Methods Using an adoptive transfer model of colitis, we compared the colitogenic potential of wild-type, interleukin-17A (IL-17A)–, IL-17F–, IL-22–, and RORγ-deficient CD4 + CD25 − T cells in RAG1-null mice. Results Adoptive transfer of IL-17A–, IL-17F–, or IL-22–deficient T…

Adoptive cell transferNeutrophilsReceptors Retinoic Acidmedicine.medical_treatmentBiologyInflammatory bowel diseasePathogenesisMiceInterferonCell MovementmedicineAnimalsIL-2 receptorColitisCells CulturedReceptors Thyroid HormoneHepatologyInterleukinsInterleukin-17GastroenterologyDendritic CellsT-Lymphocytes Helper-InducerNuclear Receptor Subfamily 1 Group F Member 3medicine.diseaseColitisAdoptive TransferMice Inbred C57BLCytokineImmunologyChronic Diseasebiology.proteinCytokinesAntibodymedicine.drugGastroenterology
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Phenotypic variability in patients with generalised resistance to thyroid hormone.

1995

Genetic linkage of generalised resistance to thyroid hormone (GRTH) to the human thyroid receptor beta 1 gene has been identified. To date 38 different mutations in several kindreds have been documented. We report on a family with GRTH displaying an adenine for guanine substitution at nucleotide 1234 resulting in a threonine for alanine substitution at codon 317 of exon 9. This mutation has been described for different phenotypes, suggesting that the heterogeneity in GRTH may be the result of multiple genetic factors.

AdultMaleThyroid Hormone Resistance SyndromeThyroid Hormonesmedicine.medical_specialtyGenetic LinkageMolecular Sequence DataThyroid Function TestsBiologymedicine.disease_causeThyroid function testsGenetic HeterogeneityExonGenetic linkageInternal medicineGeneticsmedicineHumansPoint MutationAmino Acid SequenceChildGeneGenetics (clinical)GeneticsMutationReceptors Thyroid HormoneBase Sequencemedicine.diagnostic_testGenetic heterogeneityPoint mutationThyroidPedigreePhenotypemedicine.anatomical_structureEndocrinologyChild PreschoolFemaleResearch ArticleJournal of Medical Genetics
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Cellular mechanism of action of thyroid hormones.

1987

Abstract It has emerged in the last decade that the molecular mechanism of action of thyroid hormones resembles that of steroids; thyroid hormones indeed exert their effects mainly by directly regulating gene expression, on association with specific chromatin-bound receptors. Of the two thyroid hormones, thyroxine (T4) appears to be a sort of prohormone, whereas triiodothyronine (T3) seems to be the active form; in this respect, T4-deiodination, which occurs at the level of the target tissues, may be crucial in the local homeostasis of T3. Moreover, many cellular compartments, other than the nucleus, can bind thyroid hormone, and at least some of these further sites might play some role in …

Cancer Researchmedicine.medical_specialtyThyroid HormonesTriiodothyronineReceptors Thyroid HormoneProhormoneThyroidCell BiologyBiologyChromatinEndocrinologymedicine.anatomical_structureMechanism of actionGene Expression RegulationInternal medicinemedicineAnimalsmedicine.symptomReceptorMolecular BiologyCellular compartmentDevelopmental Biologymedicine.drugHormoneDifferentiation; research in biological diversity
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Nuclear receptors modulate the interaction of Sp1 and GC-rich DNA via ternary complex formation

2000

Binding sites for transcription factor Sp1have been implicated in the transcriptional regulation of several genes by hormones or vitamins, and here we show that a GC-rich element contributes to the retinoic acid response of the interleukin 1β promoter. To explain such observations, it has been proposed that nuclear receptors can interact with Sp1 bound to GC-rich DNA. However, evidence supporting this model has remained indirect. So far, nuclear receptors have not been detected in a complex with Sp1 and GC-rich DNA, and the expected ternary complexes in non-denaturing gels were not seen. In search for these missing links we found that nuclear receptors [retinoic acid receptor (RAR), thyroid…

Cell ExtractsTranscriptional ActivationReceptors Retinoic AcidSp1 Transcription FactorRecombinant Fusion ProteinsReceptors Cytoplasmic and NuclearTretinoinRetinoic acid receptor betaBiologyRetinoid X receptorLigandsResponse ElementsTransfectionModels BiologicalBiochemistryAntibodiesCell LineSubstrate SpecificityAnimalsPromoter Regions GeneticMolecular BiologyNuclear receptor co-repressor 1Nuclear receptor co-repressor 2Binding SitesReceptors Thyroid HormoneDNACell BiologyRetinoic acid receptor gammaRetinoid X receptor gammaGC Rich SequenceProtein Structure TertiaryNuclear receptor coactivator 1Retinoic acid receptorDrosophila melanogasterEcdysteroneRetinoid X ReceptorsOligodeoxyribonucleotidesBiochemistryReceptors CalcitriolThermodynamicsResearch ArticleInterleukin-1Protein BindingTranscription FactorsBiochemical Journal
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T helper 17 lineage differentiation is programmed by orphan nuclear receptors ROR alpha and ROR gamma.

2007

T cell functional differentiation is mediated by lineage-specific transcription factors. T helper 17 (Th17) has been recently identified as a distinct Th lineage mediating tissue inflammation. Retinoic acid receptor-related orphan receptor gamma (ROR gamma) was shown to regulate Th17 differentiation; ROR gamma deficiency, however, did not completely abolish Th17 cytokine expression. Here, we report Th17 cells highly expressed another related nuclear receptor, ROR alpha, induced by transforming growth factor-beta and interleukin-6 (IL-6), which is dependent on signal transducer and activator of transcription 3. Overexpression of ROR alpha promoted Th17 differentiation, possibly through the c…

Encephalomyelitis Autoimmune ExperimentalReceptors Retinoic AcidT cellImmunologyRetinoic acidReceptors Cytoplasmic and NuclearElectrophoretic Mobility Shift AssayBiology03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineT-Lymphocyte SubsetsmedicineT helper 17 cellImmunology and AllergyAnimalsCell LineageReceptorMOLIMMUNOTranscription factor030304 developmental biologyOrphan receptor0303 health sciencesReceptors Thyroid HormoneReverse Transcriptase Polymerase Chain ReactionInterleukin-17Cell DifferentiationNuclear Receptor Subfamily 1 Group F Member 1T-Lymphocytes Helper-InducerNuclear Receptor Subfamily 1 Group F Member 3Molecular biologyMice Mutant StrainsCell biologymedicine.anatomical_structureInfectious DiseaseschemistryNuclear receptorSTAT proteinTrans-ActivatorsFemale030215 immunologyImmunity
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Resistance to thyroid hormones. Study of an affected kindred diagnosed at neonatal age

1998

Resistance to thyroid hormones (RTH) is a rare condition of reduced activity of thyroid hormones on peripheral tissues and/or reduced suppression of TSH secretion by thyroid hormones. The disease is characterised by high serum levels of T3, T4, fT3 and fT4, and by unexpectedly normal or high TSH levels. The origin of the resistance has been recognised in a thyroid hormone receptor deficit, whose gene (TRβ) has been mapped on chromosome 3p24.3 and several mutations have been identified. The clinical presentation may vary among a large spectrum from hypo-, to eu-, to hyperthyroidism in different patients, even in the same family. The diagnosis of RTH at birth and in the first months of life i…

HypothyroidismResistence to thyroid hormonesThyroid hormone receptors
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Metabolic adaptations in neonatal mother-deprived rabbits

2010

[EN] In order to study the metabolic adaptation in response to 48 h transient doe-litter separation (DLS) in young rabbits (5 rabbits/d group) between postnatal 9 and 11 d, plasma concentrations of thyroid hormones T3 and T4, insulin, leptin, glucose, triglycerides (TG), and free fatty acids (FFA) were examined before (6-8 d), during (9-11 d), and after separation (12-16 d). T3 concentrations in newborn control rabbits gradually increased from 0.6 ng/mL at postnatal 6 d to 1.0 ng/mL at postnatal 16 d, whereas those of T4 remained fairly constant (25 ng/mL) up to postnatal 14 d, when T4 gradually declined to 8 ng/mL. T3 values of DLS newborn rabbits did not differ from those of controls at p…

Leptinmedicine.medical_specialtymaternal separation thyroid hormones insulin leptin glucose rabbitsSettore AGR/19 - Zootecnica SpecialeTriiodothyronineThyroid hormonesInsulinmedicine.medical_treatmentLeptinBlood sugarRabbitBiologyGlucoseEndocrinologyInternal medicineThyroid hormonesBlood plasmaPlasma concentrationmedicineInsulinEndocrine systemAnimal Science and ZoologyMaternal separation
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