Thyroid hormone deficiency and muscle metabolism during light and heavy exercise in dogs

1988 ◽  
Vol 412 (3) ◽  
pp. 336-337 ◽  
Author(s):  
H. Kaciuba-Uścilko ◽  
Z. Brzezińska ◽  
B. Kruk ◽  
K. Nazar
Keyword(s):  
Thyroid Hormone ◽  
Muscle Metabolism ◽  
Hormone Deficiency ◽  
Heavy Exercise

Effects of postnatal thyroid hormone deficiency on neurogenesis in the juvenile and adult rat

2009 ◽  
Vol 34 (2) ◽  
pp. 366-374 ◽  
Author(s):  
Liqun Zhang ◽  
Klas Blomgren ◽  
H. Georg Kuhn ◽  
Christi M. Cooper-Kuhn
Keyword(s):  
Thyroid Hormone ◽  
Hormone Deficiency ◽  
Adult Rat

Thyroid hormone is required for the phenotype transitions induced by the pharmacological inhibition of calcineurin in adult soleus muscle of rats

2008 ◽  
Vol 294 (1) ◽  
pp. E69-E77 ◽  
Author(s):  
Nathalie Koulmann ◽  
Lahoucine Bahi ◽  
Florence Ribera ◽  
Hervé Sanchez ◽  
Bernard Serrurier ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Soleus Muscle ◽  
Hormone Deficiency ◽  
Peroxisome Proliferator ◽  
Mrna Levels ◽  
Peroxisome Proliferator Activated Receptor ◽  
Thyroid State ◽  
Novel Approach ◽  
A Subunit ◽  
Calcineurin Inhibition

The present experiment was designed to examine the effects of hypothyroidism and calcineurin inhibition induced by cyclosporin A (CsA) administration on both contractile and metabolic soleus muscle phenotypes, with a novel approach to the signaling pathway controlling mitochondrial biogenesis. Twenty-eight rats were randomly assigned to four groups, normothyroid, hypothyroid, and orally treated with either CsA (25 mg/kg, N-CsA and H-CsA) or vehicle (N-Vh and H-Vh), for 3 wk. Muscle phenotype was estimated by the MHC profile and activities of oxidative and glycolytic enzymes. We measured mRNA levels of the peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), the major regulator of mitochondrial content. We also studied the expression of the catalytic A-subunit of calcineurin (CnA) both at protein and transcript levels and mRNA levels of modulatory calcineurin inhibitor proteins (MCIP)-1 and -2, which are differentially regulated by calcineurin activity and thyroid hormone, respectively. CsA-administration induced a slow-to-fast MHC transition limited to the type IIA isoform, which is associated with increased oxidative capacities. Hypothyroidism strongly decreased both the expression of fast MHC isoforms and oxidative capacities. Effects of CsA administration on muscle phenotype were blocked in conditions of thyroid hormone deficiency. Changes in the oxidative profile were strongly related to PGC-1α changes and associated with phosphorylation of p38 MAPK. Calcineurin and MCIPs mRNA levels were decreased by both hypothyroidism and CsA without additive effects. Taken together, these results suggest that adult muscle phenotype is primarily under the control of thyroid state. Physiological levels of thyroid hormone are required for the effects of calcineurin inhibition on slow oxidative muscle phenotype.

Thyroid hormone deficiency changes the distribution of oligodendrocyte/myelin markers during oligodendroglial differentiation in vitro

2006 ◽  
Vol 24 (7) ◽  
pp. 445-453 ◽  
Author(s):  
V. Younes‐Rapozo ◽  
J. Berendonk ◽  
T. Savignon ◽  
A.C. Manhães ◽  
P.C. Barradas
Keyword(s):  
Thyroid Hormone ◽  
Hormone Deficiency

Consequences of thyroid hormone deficiency induced by the specific ablation of thyroid follicle cells in adult transgenic mice

1994 ◽  
Vol 143 (1) ◽  
pp. 107-120 ◽  
Author(s):  
H Wallace ◽  
K McLaren ◽  
R Al-Shawi ◽  
J O Bishop
Keyword(s):  
Body Weight ◽  
Thyroid Hormone ◽  
Transgenic Mice ◽  
Follicle Cells ◽  
Hormone Deficiency ◽  
Mrna Levels ◽  
Thyroid Follicle ◽  
Receptor Mrna ◽  
The Many ◽  
Tsh Levels

Abstract The herpes simplex type 1 virus thymidine kinase (HSV1-TK) reporter gene was coupled to a bovine thyroglobulin promoter (TG-tk construct). Within the thyroid glands of transgenic mice expression was confined to thyroid follicle cells. Infusion of Ganciclovir (9-[(1,3-dihydroxy-2-propoxy)methyl]guanine) to 8 to 12 week transgenic females led to the complete loss of thyroid HSV1-TK activity (at 3 to 4 days) and thyroid follicles (between 7 and 14 days). During the first 5 days of treatment a single reciprocal oscillation in circulating thyroxine (T4) and TSH levels occurred. By 14 days the circulating triiodothyronine (T3) and T4 levels of all treated animals were below the detection limits of the assays, while TSH levels were elevated ten-fold and continued to increase thereafter. During 14 days of treatment the thyroids regressed, protein content fell by 80–90% and the C cells, normally dispersed within the central region of each gland, came together in aggregates. Pituitary GH levels in females rose and fell back to normal within 14 days and between 14 and 28 days fell to a level comparable with that of GH-deficient lit/lit mice. The levels of hepatic GH receptor mRNA and the predominant 6·6 kb T3 receptor mRNA were unaffected by thyrocyte ablation. Thyrocyte ablation had no effect on the level of prolactin (Prl) receptor mRNA in females, but increased Prl receptor mRNA levels in males and eliminated group 1 major urinary protein (MUP) mRNA in females. T4 replacement reversed the effects of thyrocyte ablation on MUP mRNA in females and on Prl receptor mRNA in males. Despite the many physiological changes induced by thyrocyte ablation, ablated mice have been maintained for up to 1 year without thyroid hormone supplementation. T4-deficient females were normally fertile and carried pups to term. Although transgenic males expressed HSV1-TK ectopically in spermatids and spermatozoa at levels similar to thyrocyte levels, a rate of Ganciclovir infusion which successfully ablated the thyrocytes did not affect the testis. As an alternative to infusion by minipump, thyrocyte ablation could be achieved by 6 twice-daily injections of Ganciclovir, at a level of 112 μg Ganciclovir/g body weight per day, and fetuses in utero could be thyrocyte ablated by administering 50 or 15 μg/g body weight per day to pregnant females between days 14 and 18 of gestation. These data demonstrate the potential value of transgenic thyrocyte ablation in the study of the effects of thyroid hormone deprivation. Journal of Endocrinology (1994) 143, 107–120

scholarly journals The effect of thyroid hormone deficiency on erythropoiesis in dogs

2019 ◽  
Vol 88 (3) ◽  
pp. 257-264 ◽  
Author(s):  
Olga Aniołek
Keyword(s):  
Thyroid Hormone ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Clinical Symptoms ◽  
Cell System ◽  
Hormone Deficiency ◽  
Control Group ◽  
Average Mass ◽  
Packed Red Blood Cells ◽  
Experimental Group

This research aimed to evaluate the effect of thyroid hormone deficiency on the erythrocytic system in dogs. Dogs with clinical symptoms of hypothyreosis such as obesity, hyperpigmentation, and lethargy were selected. The dogs demonstrating breed predisposition to hypothyreosis were incorporated in the analysis: Dachshunds, Retrievers, and mixed-breed dogs. A detailed history was taken and clinical, hormonal, biochemical and haematological blood tests were performed. Peripheral blood samples were taken from 53 dogs. Finally, the dogs with the initial T4 (thyroxine) concentration < 1.3 µg/dl and animals demonstrating clinical improvement after a 2-month therapy with levothyroxine at a dose of 10 µg/kg administeredper ostwo times a day were qualified. The animals between 10 months to 13 years of age were divided into two groups: clinically healthy (control group, n = 35) and dogs presenting clinical symptoms of hypothyreosis (experimental group, n = 18). In this research, the broadly described normocytic normochromic non-regenerative anaemia was not diagnosed in dogs with hypothyreosis. However, a positive correlation between T4 and red blood cell indices such as the average mass of haemoglobin per red blood cell, concentration of haemoglobin in a given volume of packed red blood cells as well as a negative correlation with haematocrit value was discovered in the experimental group after the 2-month therapy with levothyroxine. These results point to the influence of thyroid hormones on erythropoiesis. This observation is partially consistent with other studies, which noted the casual link between the changes in red blood cell system and the function of thyroid in dogs and humans.

scholarly journals Hypothyroidism Therapy

2021 ◽  
Author(s):  
Wissal Abassi ◽  
Nejmeddine Ouerghi ◽  
Anissa Bouassida
Keyword(s):  
Coronary Artery Disease ◽  
Thyroid Hormone ◽  
Hormone Deficiency ◽  
Deficiency Anemia ◽  
Low Doses ◽  
Successful Therapy ◽  
Sympathetic Hyperactivity ◽  
Thyroxine Therapy ◽  
The Common ◽  
Artery Disease

Hypothyroidism refers to the common pathological disorder of thyroid hormone deficiency. The successful therapy for hypothyroidism is levothyroxine (LT4) administration, which is the same as thyroxine but produced synthetically. Serum thyrotropin (TSH) normalization with LT4 replacement therapy in hypothyroidism is generally needed to restore a euthyroid state. The daily dose of thyroxine therapy depends on various factors, such as body weight, age, and severity. It also differs from hypothyroidism during pregnancy to congenital hypothyroidism. The presence of various comorbidities may exist such as myxoedema coma, coronary artery disease, obesity, anemia and COVID-19 which necessitate individualized treatment. LT4 intolerance manifested with sympathetic hyperactivity may appear during the first hours after the LT4 administration. It requires starting with very low doses of LT4 that should be increased gradually, and reaching normal TSH may take several months. The sympathetic hyperactivity may be attributable to the presence of uncorrected iron-deficiency anemia that worsens by the use of thyroid hormone.

scholarly journals Thyroid Gene Mutations in Pregnant and Breastfeeding Women Diagnosed With Transient Congenital Hypothyroidism: Implications for the Offspring’s Health

2021 ◽  
Vol 12 ◽  
Author(s):  
Maria C. Opazo ◽  
Juan Carlos Rivera ◽  
Pablo A. Gonzalez ◽  
Susan M. Bueno ◽  
Alexis M. Kalergis ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Congenital Hypothyroidism ◽  
Gene Mutations ◽  
Genetic Variations ◽  
Hormone Deficiency ◽  
Iodide Transport ◽  
Transport Defect ◽  
Pregnancy And Lactation ◽  
Transient Congenital Hypothyroidism

Fetus and infants require appropriate thyroid hormone levels and iodine during pregnancy and lactation. Nature endorses the mother to supply thyroid hormones to the fetus and iodine to the lactating infant. Genetic variations on thyroid proteins that cause dyshormonogenic congenital hypothyroidism could in pregnant and breastfeeding women impair the delivery of thyroid hormones and iodine to the offspring. The review discusses maternal genetic variations in thyroid proteins that, in the context of pregnancy and/or breastfeeding, could trigger thyroid hormone deficiency or iodide transport defect that will affect the proper development of the offspring.

scholarly journals A Rare Case of 83-Year-Old Transgender Female: Can Thyroid Hormone Deficiency Be Involved in Transgenderism and Gender Dysphoria?

2020 ◽  
Vol 10 (02) ◽  
pp. 23-40
Author(s):  
Andrey Frolov ◽  
Lauren Polcaro ◽  
Craig Lawson ◽  
Yun Tan ◽  
John R. Martin III
Keyword(s):  
Thyroid Hormone ◽  
Gender Dysphoria ◽  
Rare Case ◽  
Hormone Deficiency ◽  
And Gender

scholarly journals Endocrine Deficiency As a Function of Radiation Dose to the Hypothalamus and Pituitary in Pediatric and Young Adult Patients With Brain Tumors

2018 ◽  
Vol 36 (28) ◽  
pp. 2854-2862 ◽  
Author(s):  
Ralph E. Vatner ◽  
Andrzej Niemierko ◽  
Madhusmita Misra ◽  
Elizabeth A. Weyman ◽  
Claire P. Goebel ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Young Adults ◽  
Young Adult ◽  
Thyroid Hormone ◽  
Radiation Dose ◽  
Brain Tumors ◽  
Adrenocorticotropic Hormone ◽  
Hormone Deficiency ◽  
Children And Young Adults

Purpose There are sparse data defining the dose response of radiation therapy (RT) to the hypothalamus and pituitary in pediatric and young adult patients with brain tumors. We examined the correlation between RT dose to these structures and development of endocrine dysfunction in this population. Materials and Methods Dosimetric and clinical data were collected from children and young adults (< 26 years of age) with brain tumors treated with proton RT on three prospective studies (2003 to 2016). Deficiencies of growth hormone (GH), thyroid hormone, adrenocorticotropic hormone, and gonadotropins were determined clinically and serologically. Incidence of deficiency was estimated using the Kaplan-Meier method. Multivariate models were constructed accounting for radiation dose and age. Results Of 222 patients in the study, 189 were evaluable by actuarial analysis, with a median follow-up of 4.4 years (range, 0.1 to 13.3 years), with 31 patients (14%) excluded from actuarial analysis for having baseline hormone deficiency and two patients (0.9%) because of lack of follow-up. One hundred thirty patients (68.8%) with medulloblastoma were treated with craniospinal irradiation (CSI) and boost; most of the remaining patients (n = 56) received involved field RT, most commonly for ependymoma (13.8%; n = 26) and low-grade glioma (7.4%; n = 14). The 4-year actuarial rate of any hormone deficiency, growth hormone, thyroid hormone, adrenocorticotropic hormone, and gonadotropin deficiencies were 48.8%, 37.4%, 20.5%, 6.9%, and 4.1%, respectively. Age at start of RT, time interval since treatment, and median dose to the combined hypothalamus and pituitary were correlated with increased incidence of deficiency. Conclusion Median hypothalamic and pituitary radiation dose, younger age, and longer follow-up time were associated with increased rates of endocrinopathy in children and young adults treated with radiotherapy for brain tumors.

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