scholarly journals The Predictive Role of Thyroid Hormone Levels for Early Diabetic Retinal Changes in Experimental Rat and Human Diabetes

2021 ◽  
Vol 62 (6) ◽  
pp. 20
Author(s):  
Anna Énzsöly ◽  
Rozina I. Hajdú ◽  
Zsolt Turóczi ◽  
Irén Szalai ◽  
Erika Tátrai ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Hormone Levels ◽  
Human Diabetes ◽  
Predictive Role ◽  
Thyroid Hormone Levels

scholarly journals Manipulating plasma thyroid hormone levels at hatching alters development of endothermy and ventilation in Pekin duck (Anas platyrhynchos domestica)

2020 ◽  
Vol 223 (22) ◽  
pp. jeb237701
Author(s):  
Tushar S. Sirsat ◽  
Edward M. Dzialowski
Keyword(s):  
Thyroid Hormone ◽  
Tidal Volume ◽  
Developmental Trajectory ◽  
Pekin Duck ◽  
Thyroid Peroxidase ◽  
Hormone Levels ◽  
Ventilation Frequency ◽  
Thyroid Hormone Levels ◽  
And Control

ABSTRACTAt hatching in precocial birds, there are rapid physiological and metabolic phenotypic changes associated with attaining endothermy. During the transition to ex ovo life, thyroid hormone levels naturally increase, peaking at hatching, and then decline. To better understand the role of the natural increase in thyroid hormone at hatching in regulating the developmental trajectory of the Pekin duck's endothermic phenotype, we examined development of O2 consumption (V̇O2) and ventilation (frequency, tidal volume and minute ventilation) while inhibiting the developmental increase in thyroid hormones that occurs at hatching via administration of the thyroid-peroxidase inhibitor methimazole (MMI) or accelerating the developmental increase via triiodothyronine (T3) supplementation. Animals were dosed only on day 24 of a 28-day incubation period and studied on incubation day 25, during external pipping (EP) and 1 day post-hatching (dph). On day 25, there was an increase in V̇O2 in the hyperthyroid treatment compared with the other two treatments. During the EP stage, there was a significant effect of thyroid status on V̇O2, with hyperthyroid V̇O2 being highest and hypothyroid V̇O2 the lowest. By 1 dph, the supplemented T3 and control animals had similar V̇O2 responses to cooling with comparable thermal neutral zones followed by increased V̇O2. Hypothyroid 1 dph hatchlings had a lower resting V̇O2 that did not increase to the same extent as the supplemented T3 and control animals during cooling. During EP, inhibiting the rise in T3 resulted in embryos with lower ventilation frequency and tidal volume than control and supplemented T3 embryos. At 1 dph, ventilation frequency of all animals increased during cooling, but tidal volume only increased in supplemented T3 and control hatchlings. Our data support the role of the late incubation increase in T3 in regulating the systemic development of endothermic metabolic capacity and associated control of ventilation occurring at hatching of the Pekin duck.

STUDIES ON THE ORIGIN OF ALTERED THYROID HORMONE LEVELS IN THE BLOOD OF RATS DURING COLD EXPOSURE

1979 ◽  
Vol 91 (3) ◽  
pp. 484-492 ◽  
Author(s):  
C. van Hardeveld ◽  
M. J. Zuidwijk ◽  
A. A. H. Kassenaar
Keyword(s):  
Thyroid Hormone ◽  
Cold Exposure ◽  
Plasma Levels ◽  
Dose Regimen ◽  
Sympathetic Activity ◽  
Chemical Sympathectomy ◽  
Hormone Levels ◽  
Thyroid Hormone Levels ◽  
Altered Thyroid

ABSTRACT The effect of sympathetic activity on T4 and T3 levels in cold-exposed rats was investigated. Administration of the highest dose of propranolol (2 mg/100 g b.w.) twice daily during 4 days decreased T4 and T3 concentrations in plasma of rats living at 23°C (T4 from 46.4 ± 2.6 to 25.8 ± 5.3 nmol/l and T3 from 1.08. ± 0.6 to 0.82 ± 0.12 nmol/l). No significant effect on T4 and T3 levels (49.0 ± 11.6 and 1.48 ± 0.16 n/mol, respectively) after the administration of the same dose regimen of propranolol was observed in rats exposed to cold for 4 weeks. T4 and T3 levels in rats exposed to cold for 4 weeks were not significantly altered 1 week after sympathectomy, while remaining in the cold. However, chemical sympathectomy before cold exposure delayed the cold induced T3 elevation occurring during the first week of cold exposure (controls: from 1.16 ± 0.19 to 1.44 ± 0.29 nmol/l; sympathectomized rats: from 1.07 ± 0.12 to 1.17 ± 0.22 nmol/l). After 2 weeks of cold exposure the T3 levels of controls and sympathectomized rats were not significantly different (controls: 1.45 ± 0.12 nmol/l, sympathectomized rats: 1.38 ± 0.15 nmol/l). No effect of sympathectomy was observed on T4 levels. These experiments show that the role of sympathetic activity in increasing T3 is not clear during cold exposure. They provide some evidence that sympathetic activity may play a role in the initiation of the process leading to increased T3 plasma levels during cold exposure.

scholarly journals Analysis of Hypothalamic TRH Neurons in Regulating Thyroid Hormone Levels

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A849-A849
Author(s):  
Ricardo H Costa e Sousa ◽  
Rodrigo Rorato ◽  
Anthony Neil Hollenberg ◽  
Kristen R Vella
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormone Receptor ◽  
Designer Drugs ◽  
Mrna Levels ◽  
Hormone Levels ◽  
Males And Females ◽  
Thyroid Hormone Levels ◽  
Hpt Axis ◽  
Tsh Levels

Abstract Thyroid hormone (TH) is a major regulator of development and metabolism. An important mechanism controlling TH production is the negative feedback at the hypothalamic and pituitary level and it has been suggested that thyroid hormone receptor β (TRβ) is the main mediator of TH actions in the hypothalamic paraventricular nucleus (PVN). Nevertheless, the direct actions of TH and TRβ in the negative regulation of TRH have yet to be demonstrated in vivo. Here we used two approaches to investigate the TRH neuron. First, we used a chemogenetic tool to directly investigate the role of TRH neurons on the regulation of thyroid hormone levels. Mice expressing Cre-recombinase in TRH neurons received bilateral injections of the activating designer receptors exclusively activated by designer drugs (DREADD) directly into the PVN. Activation of TRH neurons produced a rapid and sustained increase in circulating TSH levels in both males and females. TSH levels increased approximately 10-fold from baseline within 15 minutes of injection of CNO, returning to baseline within 2.5 hours. TH levels were increased approximately 2-fold in males and females. Therefore, using a chemogenetic approach, we were able to directly evaluated the role of PVN TRH neurons on the control of thyroid activity, for the first time. Next, we generated mice deficient in TRβ specifically in neurons expressing melanocortin 4 receptor (MC4R), which overlaps with TRH expression in the PVN. Knockout mice (KO) developed normally and showed no change in TH and TSH levels. TRH mRNA levels in the PVN of KO mice were similar to control mice. To investigate if the deletion of TRβ in the PVN changes the sensitivity of the HPT axis to T3, mice were rendered hypothyroid and given increasing doses of T3 for 2 weeks. Results show no difference in TRH mRNA or serum TSH between controls and KO. Surprisingly, despite the presence of detectable genomic recombination on the TRβ gene in the PVN, there was no difference in TRβ mRNA expression between control and KO mice, suggesting that either MC4R-positive neurons do not express TRβ or they represent a very small population of TRβ-positive cells in the PVN. Present data show that TRH neuron activation rapidly stimulates TSH release and increases TH levels, demonstrating a major role of these neurons in the regulation of the hypothalamic-pituitary-thyroid (HPT) axis. Nevertheless, deletion of TRβ from MC4R neurons had no major effect on either TRH or TH levels in in mice. Additionally, TRβ in MC4R-positive TRH neurons in the PVN is not necessary for TH-induced suppression of TRH mRNA. Although further studies are necessary, these data suggest that there are distinct populations of hypophysiotropic TRH neurons in the PVN, some of which are not regulated by thyroid hormone and TRβ.

scholarly journals Iodothyronine deiodinases and the control of plasma and tissue thyroid hormone levels in hyperthyroid tilapia (Oreochromis niloticus)

2005 ◽  
Vol 184 (3) ◽  
pp. 467-479 ◽  
Author(s):  
S Van der Geyten ◽  
N Byamungu ◽  
G E Reyns ◽  
E R Kühn ◽  
V M Darras
Keyword(s):  
Thyroid Hormone ◽  
Oreochromis Niloticus ◽  
Degradation Mechanism ◽  
Current Data ◽  
Type I ◽  
Iodothyronine Deiodinase ◽  
Hormone Levels ◽  
Thyroid Hormone Levels

Thyroid status is one of the most potent regulators of peripheral thyroid hormone metabolism in vertebrates. Despite this, the few papers that have been published concerning the role of thyroid hormones in the regulation of thyroid function in fish often offer conflicting data. We therefore set out to investigate the effects of tetraiodothyronine (thyroxine) (T4) or tri-iodothyronine (T3) supplementation (48 p.p.m.) via the food on plasma and tissue thyroid hormone levels as well as iodothyronine deiodinase (D) activities in the Nile tilapia (Oreochromis niloticus). T4 supplementation did not induce a hyperthyroid state and subsequently had no effects on the thyroid hormone parameters measured, with the liver as the sole notable exception. In T4-fed tilapias, the hepatic T4 levels increased substantially, and this was accompanied by an increase in in vitro type I deiodinase (D1) activity. Although the lack of effect of T4 supplementation could be partially explained by an inefficient uptake of T4 from the gut, our current data suggest that also the increased conversion of T4 into reverse (r)T3 by the D1 present in the liver plays an important role in this respect. In addition, T3 supplementation increased plasma T3 and decreased plasma T4 concentrations. T3 levels were also increased in the liver, brain, kidney, gill and white muscle, but without affecting local T4 concentrations. However, this increase in T3 availability remained without effect on D1 activity in liver and kidney. This observation, together with the 6-n-propylthiouracyl (PTU) insensitivity of the D1 enzyme in fish, sets the D1 in teleost fish clearly apart from its mammalian and avian counterparts. The changes in hepatic deiodinases confirm the role of the liver as an important T3-regulating tissue. However, the very short plasma half-life of exogenously administered T3 implies the existence of an efficient T3 clearing/degradation mechanism other than deiodination.

Altered thyroid hormone levels in bacterial sepsis: The role of nutritional adequacy

Metabolism ◽  
1980 ◽  
Vol 29 (10) ◽  
pp. 936-942 ◽  
Author(s):  
David A. Richmand ◽  
Mark E. Molitch ◽  
Thomas F. O'Donnell
Keyword(s):  
Thyroid Hormone ◽  
Bacterial Sepsis ◽  
Nutritional Adequacy ◽  
Hormone Levels ◽  
Thyroid Hormone Levels ◽  
Altered Thyroid

scholarly journals DIAGNOSIS OF ENDOCRINE DISEASE: How reliable are free thyroid and total T3 hormone assays?

2016 ◽  
Vol 175 (6) ◽  
pp. R255-R263 ◽  
Author(s):  
Kerry J Welsh ◽  
Steven J Soldin
Keyword(s):  
Thyroid Hormone ◽  
Reference Method ◽  
Reference Interval ◽  
Thyroid Stimulating Hormone ◽  
Hormone Levels ◽  
Disease States ◽  
Number Of Patients ◽  
Liquid Chromatography Tandem Mass ◽  
Thyroid Hormone Levels

Hypothyroidism is a very common disorder worldwide, for which the usual treatment is monotherapy with levothyroxine (L-T4). However, a number of patients treated with L-T4 continue to report symptoms of hypothyroidism despite seemingly normal levels of thyroid-stimulating hormone (TSH), free-T3 (FT3) and free-T4 (FT4) measured by immunoassay. This review summarizes the limitations of the immunoassays commonly used to measure thyroid hormone levels and emphasizes the advantages of the role of liquid chromatography-tandem mass spectrometry (LC-MS/MS). Immunoassays for free thyroid hormone are affected by alterations in serum binding proteins that occur in many physiological and disease states. Multiple studies show falsely normal values for T3, FT3 and FT4 by immunoassay that are below the reference interval when measured by (ultrafiltration) LC-MS/MS, a reference method. We suggest evaluation of thyroid hormone levels by ultrafiltration LC-MS/MS for patients who continue to experience hypothyroid symptoms on LT-4. This may help identify the approximately 20% subset of patients who would benefit from addition of T3 to their treatment regimen (combination therapy).

scholarly journals Transient Hypothyroxinemia in Preterm Infants: The Role of Cord Sera Thyroid Hormone Levels Adjusted for Prenatal and Intrapartum Factors

2005 ◽  
Vol 90 (8) ◽  
pp. 4599-4606 ◽  
Author(s):  
Fiona L. R. Williams ◽  
Gary J. Mires ◽  
Carol Barnett ◽  
Simon A. Ogston ◽  
Hans van Toor ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Preterm Infants ◽  
Hormone Levels ◽  
Thyroid Hormone Levels ◽  
Intrapartum Factors

scholarly journals Role of thyroid metabolism in vestibular vertigo

2020 ◽  
Vol 6 (2) ◽  
pp. 359
Author(s):  
Anisa . ◽  
Sheetal Rai
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Control Group ◽  
Large Sample Size ◽  
Thyroid Function Tests ◽  
Hormone Levels ◽  
Thyroid Metabolism ◽  
Thyroid Hormone Levels ◽  
Altered Thyroid

<p class="abstract"><strong>Background:</strong> Thyroid hormones play a role in the development and functioning of the inner ear.  Therefore, it was hypothesized that a derangement in the thyroid hormone levels can affect the cochleo-vestibular system.</p><p class="abstract"><strong>Methods:</strong> The present study included 64 cases and 64 controls. All patients diagnosed with peripheral vertigo were enrolled into the study. All the subjects underwent thyroid function tests- serum T3, T4 and thyroid stimulating hormone (TSH). Free hormone levels were obtained in patients with subclinical hypo or hyperthyroidism. The data was analyzed using Independent sample t test.  </p><p class="abstract"><strong>Results:</strong> Out of 64 cases only 10 patients showed altered thyroid values. Fifty-nine cases were diagnosed with benign paroxysmal positional vertigo (BPPV) out of which 9 (15%) had altered thyroid hormone levels. Among the control group, 12 were found to have deranged thyroid hormone levels.</p><p class="abstract"><strong>Conclusions:</strong> There is no association between functional thyroid hormone levels and BPPV. Therefore, altered thyroid metabolism has no role in the causation of vestibular dysfunction due to BPPV. However, in case of Meniere’s disease and Vestibular neuronitis further studies with large sample size are required to ascertain the role of functional thyroid hormones in producing vestibular symptoms.</p>

scholarly journals GENETICS IN ENDOCRINOLOGY: Genetic variation in deiodinases: a systematic review of potential clinical effects in humans

2014 ◽  
Vol 171 (3) ◽  
pp. R123-R135 ◽  
Author(s):  
Herman Verloop ◽  
Olaf M Dekkers ◽  
Robin P Peeters ◽  
Jan W Schoones ◽  
Johannes W A Smit
Keyword(s):  
Systematic Review ◽  
Genetic Variation ◽  
Thyroid Hormone ◽  
Cochrane Library ◽  
Publication Date ◽  
Clinical Effects ◽  
Hormone Levels ◽  
Serum Thyroid Hormone ◽  
Thyroid Hormone Levels

Iodothyronine deiodinases represent a family of selenoproteins involved in peripheral and local homeostasis of thyroid hormone action. Deiodinases are expressed in multiple organs and thyroid hormone affects numerous biological systems, thus genetic variation in deiodinases may affect multiple clinical endpoints. Interest in clinical effects of genetic variation in deiodinases has clearly increased. We aimed to provide an overview for the role of deiodinase polymorphisms in human physiology and morbidity. In this systematic review, studies evaluating the relationship between deiodinase polymorphisms and clinical parameters in humans were eligible. No restrictions on publication date were imposed. The following databases were searched up to August 2013: Pubmed, EMBASE (OVID-version), Web of Science, COCHRANE Library, CINAHL (EbscoHOST-version), Academic Search Premier (EbscoHOST-version), and ScienceDirect. Deiodinase physiology at molecular and tissue level is described, and finally the role of these polymorphisms in pathophysiological conditions is reviewed. Deiodinase type 1 (D1) polymorphisms particularly show moderate-to-strong relationships with thyroid hormone parameters, IGF1 production, and risk for depression. D2 variants correlate with thyroid hormone levels, insulin resistance, bipolar mood disorder, psychological well-being, mental retardation, hypertension, and risk for osteoarthritis. D3 polymorphisms showed no relationship with inter-individual variation in serum thyroid hormone parameters. One D3 polymorphism was associated with risk for osteoarthritis. Genetic deiodinase profiles only explain a small proportion of inter-individual variations in serum thyroid hormone levels. Evidence suggests a role of genetic deiodinase variants in certain pathophysiological conditions. The value for determination of deiodinase polymorphism in clinical practice needs further investigation.

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