Search results for " Thyroid Hormone"

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…

Thyroid hormone induction of the adrenoleukodystrophy-related gene (ABCD2).

2003

X-linked adrenoleukodystrophy (X-ALD) is a demyelinating disorder associated with impaired very-long-chain fatty-acid (VLCFA) beta-oxidation caused by mutations in the ABCD1 (ALD) gene that encodes a peroxisomal membrane ABC transporter. ABCD2 (ALDR) displays partial functional redundancy because when overexpressed, it is able to correct the X-ALD biochemical phenotype. The ABCD2 promoter contains a putative thyroid hormone-response element conserved in rodents and humans. In this report, we demonstrate that the element is capable of binding retinoid X receptor and 3,5,3'-tri-iodothyronine (T3) receptor (TRbeta) as a heterodimer and mediating T3 responsiveness of ABCD2 in its promoter conte…

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…

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 …

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…

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.

The nuclear receptor PPARγ selectively inhibits Th17 differentiation in a T cell–intrinsic fashion and suppresses CNS autoimmunity

2009

T helper cells secreting interleukin (IL)-17 (Th17 cells) play a crucial role in autoimmune diseases like multiple sclerosis (MS). Th17 differentiation, which is induced by a combination of transforming growth factor (TGF)-beta/IL-6 or IL-21, requires expression of the transcription factor retinoic acid receptor-related orphan receptor gamma t (ROR gamma t). We identify the nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR gamma) as a key negative regulator of human and mouse Th17 differentiation. PPAR gamma activation in CD4(+) T cells selectively suppressed Th17 differentiation, but not differentiation into Th1, Th2, or regulatory T cells. Control of Th17 differentia…

Expression of thyroid hormone receptor isoforms in the hypertrophic heart of spontaneously hypertensive rats

2001

Thyroid hormones (THs) enhance MHC alpha gene- and repress MHC beta gene-transcription in the heart, by interacting with specific nuclear receptors (TRs), that bind to regulatory sequences localized upstream of basal promoter of myosin heavy chain (MHC) genes. The overall effects of THs include an increase in V1- and a decrease in V3-myosin isozyme concentration in the heart. Myosin V1 contains two MHC alpha chains and has a higher ATPase activity than V3 isoform, which contains two beta chains. Previous studies on papillary muscles of spontaneously hypertensive rats (SHRs) showed that heart hypertrophy is accompanied by a shift from alpha to beta MHC accumulation. The present study was aim…

EFFECTS OF THYROID HORMONES ON RNA-BINDING PROTEINS EXPRESSED IN DEVELOPING RAT BRAIN

2005

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…