Manipulation of thyroid hormones in ruminants - a tool to understand their physiological role and identify their potential for increasing production efficiency

2002 ◽  
Vol 53 (3) ◽  
pp. 259 ◽  
Author(s):  
D. Villar ◽  
S. M. Rhind ◽  
J. R. Arthur ◽  
P. J. Goddard
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Production Efficiency ◽  
Hormone Replacement ◽  
Animal Health ◽  
Hormone Secretion ◽  
Plasma Concentrations ◽  
Physiological Role ◽  
Antithyroid Drugs ◽  
Few Data

Manipulations of thyroid hormone secretion and function can be used to cure thyroidal deficiencies or overactivity and as a tool to investigate their physiological roles and identify potential protocols for enhancing animal performance. An essential approach to the investigation of thyroid hormone action involves the induction of hypothyroidal states. Methods of inducing hypothyroidal states in ruminants include thyroidectomy and treatment with thionamides. There are few data concerning the induction of an optimal degree of hypothyroidism for the study of thyroid function in ruminants, unlike the situation in rodents. The effects of hypothyroidism on the physiology of ruminants, and the relative merits of thyroidectomy or of treatment with thionamides to manipulate thyroid hormone profiles in them, are reviewed and discussed. Thyroidectomy in ruminants induces an acute, irreversible, hypothyroidal state. It also has indirect, predominantly adverse, effects on many physiological processes and impairs health. Thus, thyroidectomised (THX) animals cannot be sustained for long-term studies without thyroid hormone replacement. Antithyroid drugs of the thionamide class, on the other hand, have been used with success to induce varying degrees of hypothyroidism, predominantly less severe than those induced by thyroidectomy. The changes induced by drugs are reversible upon withdrawal of treatment. However, treatment may require daily administration of the drug for several weeks before stable plasma concentrations of thyroid hormone are achieved. Furthermore, at high doses, these drugs can have toxic side effects. It is concluded that the treatment regime of choice will depend on the objectives of the individual study. Knowledge of the activities of thyroid hormone metabolising, deiodinase enzymes in the target tissues is also required if the actions of some of these drugs, their physiological roles in modulation of the thyroid hormones, and, crucially, their potential effects on animal health and production are to be properly understood and exploited.

Thyroid hormone concentrations in the plasma of fed and fasted Brahman and Hereford steers

1994 ◽  
Vol 34 (4) ◽  
pp. 439
Author(s):  
JC O'Kelly ◽  
WG Spiers
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Plasma Concentrations ◽  
Free T4 ◽  
Rumen Metabolism ◽  
Body Tissues ◽  
Breed Differences ◽  
Feeding Regimes ◽  
Ad Libitum ◽  
Brahman Steers

Plasma concentration patterns of thyroxine (TJ, free T4 (FT4), triiodothyronine (T3), and free T3 (FT3) were determined in Brahman steers fed lucerne hay ad libitum and in Brahman and Hereford steers fed restricted intakes of lucerne hay at the rate of either 208 g/h before fasting for 72 h or 250 g/h before fasting for 96 h. In Brahmans fed ad libitum, the plasma concentrations of all thyroid hormone fractions were significantly (P<0.01) correlated with one another and with feed intake. Within breeds, the concentrations of thyroid hormones were higher (P<0.001) when animals were fed at 250 g k than at 208 g/h. During both hourly feeding regimes T4, FT4, T3, and FT3 concentrations were higher (P<0.001) in Brahmans than in Herefords. Fasting after both hourly feeding regimes lowered (P<0.001) the concentrations of T4 about 53% in Brahmans and 30% in Herefords, while FT4, T3, and FT3 were lowered about 68% in Brahmans and 50% in Herefords. Consequently, thyroid hormone concentrations were significantly lower in Brahmans than in Herefords after 72 h fasting but did not differ significantly between breeds after 96 h fasting. The present results, together with those of our previous work showing breed differences in rumen metabolism, support the concept that, in Hereford and Brahman steers fed the same amount of hay in a thermoneutral environment, breed differences in plasma concentrations of thyroid hormones originate from quantitative differences in the supply of nutrients from the rumen to body tissues.

Immunization against vasoactive intestinal peptide does not affect thyroid hormone secretion or thyroid blood flow

1994 ◽  
Vol 266 (6) ◽  
pp. E905-E913
Author(s):  
M. Michalkiewicz ◽  
L. J. Huffman ◽  
M. Dey ◽  
G. A. Hedge
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Vasoactive Intestinal Peptide ◽  
Iodine Deficiency ◽  
Binding Capacity ◽  
Hormone Secretion ◽  
Passive Immunization ◽  
Male Rats ◽  
Blood Levels ◽  
Blood Flows

Vasoactive intestinal peptide (VIP) is present in thyroid parasympathetic nerves. To assess the involvement of endogenous VIP in the regulation of thyroid function, blood levels of thyroid hormones and thyroid blood flows (TBF) were measured after systemic immunization against VIP or after transection of the superior laryngeal nerves in male rats, which reduced the thyroid content of VIP but did not affect blood levels of thyroid hormones or TBF. Anti-VIP monoclonal antibody or anti-VIP serum was used for immunization against VIP in normal rats. In addition, VIP antibody was given to rats fed an iodine-deficient diet for 5 days to examine the involvement of this peptide in iodine deficiency-induced increases in TBF. Effects were measured at different times (90 s, 30 min, 1 h, and 5 days) after immunoneutralization, but none of these treatments changed blood levels of thyroid hormones or TBF in normal or iodine-deficient rats. However, passive immunization against VIP was associated with a high binding capacity of rat plasma to VIP, and this treatment reduced blood levels of prolactin as well as blood flows to the duodenum, stomach, and lung. These findings suggest that the VIP present in thyroid nerves is not involved in maintaining basal thyroid hormone secretion or TBF and that this neuropeptide does not mediate thyroid vascular adjustments to dietary iodine deficiency.

Effects of intrathyroidal metabolism of thyroxine on thyroid hormone secretion: increased degradation of thyroxine in mouse thyroids stimulated chronically with thyrotrophin

1984 ◽  
Vol 105 (1) ◽  
pp. 57-65 ◽  
Author(s):  
Ken Kubota ◽  
Hidemasa Uchimura ◽  
Tomoaki Mitsuhashi ◽  
Shoo Cheng Chiu ◽  
Nobuaki Kuzuya ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Hormone Secretion ◽  
Plasma Concentrations ◽  
Experimental Period ◽  
Physiological Significance ◽  
The Media ◽  
Bovine Tsh ◽  
Tsh Levels ◽  
Mouse Thyroid

Abstract. Mice were infused continuously with graded doses of bovine TSH (bTSH) and changes in plasma concentrations of bTSH and T4 were measured. Then mice infused with 100 mU TSH per day were sacrificed on days 0, 1, 3 and 5 and their thyroids were excised to determine in vitro secretion of T4, T3 and rT3 during 3 h of incubation. At the end of the incubation, thyroidal contents of T4, T3 and rT3 were also determined after pronase digestion. Plasma bTSH levels were increased on day 1 to a level of 110 μU/ml and remained unchanged thereafter. Plasma T4 concentrations increased approximately 2-fold on day 1, but decreased to initial levels on days 3 and 5. Changes in T4 secretion in vitro paralleled those in plasma T4 concentrations; T4 secretion increased 2-fold on day 1, and decreased to the pre-TSH levels on days 3 and 5. In contrast, T3 secretion increased throughout the experimental period. The T3/T4 ratio in thyroidal secretion in vitro was the same as that in thyroidal contents on days 0 and 1 of TSH infusion, but the former was significantly greater than the latter on days 3 and 5. PTU (5.9 × 10−5 m), a known inhibitor of T4 deiodination, added to the incubation media did not affect T4 secretion on days 0 and 1, but increased T4 secretion on days 3 and 5 to the level of day 1, but did not affect T3 secretion. In the presence of PTU, the T3/T4 ratio in thyroidal secretion did not differ from that in thyroidal contents throughout the experimental period. Secretion of rT3 was increased on days 3 and 5 and PTU augmented this increase. Thyroidal content of rT3 was much increased on days 3 and 5. In contrast, methimazole (10−3 m), which does not inhibit in vitro T4 deiodination, added to the incubation media did not affect T4, T3 and rT3 secretion in vitro. When [125I]T4 was added to the media and incubated with mouse thyroid, no labelled products of T4-deiodination were observed to appear in the media even in mice infused with TSH for 5 days. These results suggest that intrathyroidal metabolism of T4 has physiological significance in controlling thyroid hormone secretion at least in TSH-stimulated thyroids.

scholarly journals Physiological Role and Use of Thyroid Hormone Metabolites - Potential Utility in COVID-19 Patients

2021 ◽  
Vol 12 ◽  
Author(s):  
Eleonore Fröhlich ◽  
Richard Wahl
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Virus Disease ◽  
Physiological Role ◽  
Promising Candidate ◽  
Reverse T3 ◽  
Metabolic Dysregulation ◽  
Main Effects ◽  
Potential Use

Thyroxine and triiodothyronine (T3) are classical thyroid hormones and with relatively well-understood actions. In contrast, the physiological role of thyroid hormone metabolites, also circulating in the blood, is less well characterized. These molecules, namely, reverse triiodothyronine, 3,5-diiodothyronine, 3-iodothyronamine, tetraiodoacetic acid and triiodoacetic acid, mediate both agonistic (thyromimetic) and antagonistic actions additional to the effects of the classical thyroid hormones. Here, we provide an overview of the main factors influencing thyroid hormone action, and then go on to describe the main effects of the metabolites and their potential use in medicine. One section addresses thyroid hormone levels in corona virus disease 19 (COVID-19). It appears that i) the more potently-acting molecules T3 and triiodoacetic acid have shorter half-lives than the less potent antagonists 3-iodothyronamine and tetraiodoacetic acid; ii) reverse T3 and 3,5-diiodothyronine may serve as indicators for metabolic dysregulation and disease, and iii) Nanotetrac may be a promising candidate for treating cancer, and resmetirom and VK2809 for steatohepatitis. Further, the use of L-T3 in the treatment of severely ill COVID-19 patients is critically discussed.

scholarly journals Sexual dimorphism in the acute effects of secondhand smoke on thyroid hormone secretion, inflammatory markers and vascular function

2008 ◽  
Vol 294 (2) ◽  
pp. E456-E462 ◽  
Author(s):  
Andreas D. Flouris ◽  
Giorgos S. Metsios ◽  
Athanasios Z. Jamurtas ◽  
Yiannis Koutedakis
Keyword(s):  
Blood Pressure ◽  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Systolic Blood Pressure ◽  
Inflammatory Cytokines ◽  
Secondhand Smoke ◽  
Vascular Function ◽  
Hormone Secretion ◽  
Gonadal Hormones ◽  
Free Thyroxine

Experimental evidence for the physiological effects of secondhand smoke (SHS) is limited, although it affects millions of people globally and its prevalence is increasing, despite currently adopted antismoking measures. Also, scarce evidence suggests that the effects of SHS may be more pronounced in men. We conducted a randomized single-blind crossover study to investigate the sex-specific SHS effects in a controlled simulated bar/restaurant environment on gonadal and thyroid hormones, inflammatory cytokines, and vascular function. Twenty-eight (women = 14) nonsmoking adults underwent a 1-h exposure to moderate SHS and a 1-h control trial. Serum and urine cotinine, gonadal and thyroid hormones, inflammatory cytokines, heart rate, and arterial blood pressure were assessed before exposure and immediately after in both trials. Results showed that testosterone ( P = 0.019) and progesterone ( P < 0.001) in men and 17β-estradiol ( P = 0.001) and progesterone ( P < 0.001) in women were significantly decreased after SHS. In men, SHS was accompanied by increased free thyroxine ( P < 0.001), triiodothyronine ( P = 0.020), and decreased the triiodothyronine-to-free thyroxine ratio ( P = 0.033). In women, significant SHS-induced change was observed only in free thyroxine ( P = 0.010), with considerable sex variation in free thyroxine and triiodothyronine and a decrease in luteinizing hormone ( P = 0.026) and follicle-stimulating hormone ( P < 0.001). After SHS, IL-1β ( P = 0.001) and systolic blood pressure ( P = 0.040) were increased in men but not women. We concluded that a 1-h SHS exposure at bar/restaurant levels is accompanied by decrements in gonadal hormones in both sexes and marked increases in thyroid hormone secretion, IL-1β production, and systolic blood pressure in men.

Causes and laboratory investigation of hypothyroidism

2011 ◽  
pp. 530-537 ◽  
Author(s):  
Ferruccio Santini ◽  
Aldo Pinchera
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Hormones ◽  
Thyroid Hormone Receptor ◽  
Hormone Secretion ◽  
Thyroid Tissue ◽  
Clinical Manifestations ◽  
Primary Hypothyroidism ◽  
Central Hypothyroidism ◽  
Resistance To Thyroid Hormones

Hypothyroidism is the clinical state that develops as a result of the lack of action of thyroid hormones on target tissues (1). Hypothyroidism is usually due to impaired hormone secretion by the thyroid, resulting in reduced concentrations of serum thyroxine (T4) and triiodothyronine (T3). The term primary hypothyroidism is applied to define the thyroid failure deriving from inherited or acquired causes that act directly on the thyroid gland by reducing the amount of functioning thyroid tissue or by inhibiting thyroid hormone production. The term central hypothyroidism is used when pituitary or hypothalamic abnormalities result in an insufficient stimulation of an otherwise normal thyroid gland. Both primary and central hypothyroidism may be transient, depending on the nature and the extent of the causal agent. Hypothyroidism following a minor loss of thyroid tissue can be recovered by compensatory hyperplasia of the residual gland. Similarly, hypothyroidism subsides when an exogenous inhibitor of thyroid function is removed. Peripheral hypothyroidism may also arise as a consequence of tissue resistance to thyroid hormones due to a mutation in the thyroid hormone receptor. Resistance to thyroid hormones is a heterogeneous clinical entity with most patients appearing to be clinically euthyroid while some of them have symptoms of thyrotoxicosis and others display selected signs of hypothyroidism. The common feature is represented by pituitary resistance to thyroid hormones, leading to increased secretion of thyrotropin that in turn stimulates thyroid growth and function. The variability in clinical manifestations depends on the severity of the hormonal resistance, the relative degree of tissue hyposensitivity, and the coexistence of associated genetic defects (see Chapter 3.4.8).

scholarly journals Impact of Monocarboxylate Transporter-8 Deficiency on the Hypothalamus-Pituitary-Thyroid Axis in Mice

Endocrinology ◽  
2010 ◽  
Vol 151 (10) ◽  
pp. 5053-5062 ◽  
Author(s):  
Marija Trajkovic-Arsic ◽  
Julia Müller ◽  
Veerle M. Darras ◽  
Claudia Groba ◽  
Sooyeon Lee ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Hormone Replacement ◽  
Hormone Secretion ◽  
High Serum ◽  
Monocarboxylate Transporter ◽  
Neurological Deficits ◽  
Serum Concentrations ◽  
Hormone Production ◽  
Serum T3

In patients, inactivating mutations in the gene encoding the thyroid hormone-transporting monocarboxylate transporter 8 (Mct8) are associated with severe mental and neurological deficits and disturbed thyroid hormone levels. The latter phenotype characterized by high T3 and low T4 serum concentrations is replicated in Mct8 knockout (ko) mice, indicating that MCT8 deficiency interferes with thyroid hormone production and/or metabolism. Our studies of Mct8 ko mice indeed revealed increased thyroidal T3 and T4 concentrations without overt signs of a hyperactive thyroid gland. However, upon TSH stimulation Mct8 ko mice showed decreased T4 and increased T3 secretion compared with wild-type littermates. Moreover, similar changes in the thyroid hormone secretion pattern were observed in Mct8/Trhr1 double-ko mice, which are characterized by normal serum T3 levels and normal hepatic and renal D1 expression in the presence of very low T4 serum concentrations. These data strongly indicate that absence of Mct8 in the thyroid gland affects thyroid hormone efflux by shifting the ratio of the secreted hormones toward T3. To test this hypothesis, we generated Mct8/Pax8 double-mutant mice, which in addition to Mct8 lack a functional thyroid gland and are therefore completely athyroid. Following the injection of these animals with either T4 or T3, serum analysis revealed T3 concentrations similar to those observed in Pax8 ko mice under thyroid hormone replacement, indicating that indeed increased thyroidal T3 secretion in Mct8 ko mice represents an important pathogenic mechanism leading to the high serum T3 levels.

LONG-TERM CONTROL OF THYROTOXICOSIS WITH THE BETA-BLOCKER SOTALOL - A MODEL OF UNTREATED HYPERTHYROIDISM?

1978 ◽  
Vol 87 (4) ◽  
pp. 734-742 ◽  
Author(s):  
Peter Wahlberg ◽  
Sten-Anders Carlsson
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Function ◽  
Beta Blocker ◽  
Clinical Symptoms ◽  
Symptom Control ◽  
Hormone Secretion ◽  
Antithyroid Drugs ◽  
Beta Blockade ◽  
Trh Stimulation

ABSTRACT Five patients with hyperthyroidism and no goitre were treated only by beta blockade with sotalol. All but one became clinically euthyroid, although the thyroid hormone values in their sera remained high. The TSH response to intravenous TRH remained absent. One patient had fluctuating thyroid hormone values, one has had borderline values for 20 months, one had a hormonal recovery within 6 months, one became clinically thyrotoxic and was switched to carbimazole, and one who had first been treated with carbimazole and had a relapse of high hormone values at 3 months and of clinical symptoms within 9 months after cessation of carbimazole treatment became clinically euthyroid with beta blockade. Sotalol offers a symptom control of hyperthyroidism without lowering the thyroid function, and thus makes it possible to study the long-term hormonal pattern of hyperthyroidism without suppression of thyroid hormone secretion. The results show that the course of hyperthyroidism may vary in duration and pattern. TRH stimulation may cause none or a small TSH response even when the disease is in hormonal remission. The cause of this phenomenon is discussed. The duration of hyperthyroidism cannot be forecast by present methods, and this should be borne in mind when patients are treated with antithyroid drugs for this disorder.

scholarly journals Thyroid Hormones Decrease Plasma 1α,25-Dihydroxyvitamin D Levels Through Transcriptional Repression of the Renal 25-Hydroxyvitamin D3 1α-Hydroxylase Gene (CYP27B1)

Endocrinology ◽  
2013 ◽  
Vol 154 (2) ◽  
pp. 609-622 ◽  
Author(s):  
Mina Kozai ◽  
Hironori Yamamoto ◽  
Mariko Ishiguro ◽  
Nagakatsu Harada ◽  
Masashi Masuda ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Gene Transcription ◽  
Transcriptional Repression ◽  
Transcriptional Activity ◽  
Plasma Concentrations ◽  
Mrna Levels ◽  
Dihydroxyvitamin D ◽  
Low Calcium Diet ◽  
Low Calcium

The primary determinant of circulating 1α,25-dihydroxyvitamin D (1,25[OH]2D) levels is the activity of 25-hydroxyvitamin D-1α-hydroxylase (cytochrome P450 27B1 [CYP27B1]) in the kidney. Hyperthyroid patients have been reported to have low levels of plasma 1,25(OH)2D. However, the detailed mechanism of thyroid hormone action on vitamin D metabolism is still poorly understood. The present study determined whether renal CYP27B1 gene expression was negatively regulated by thyroid hormones. T3-induced hyperthyroid mice showed marked decreases in plasma 1,25(OH)2D levels and in renal expression of CYP27B1 mRNA but no changes in plasma concentrations of calcium, PTH, or fibroblast growth factor-23. In addition, we observed that T3 administration significantly decreased plasma 1,25(OH)2D and renal CYP27B1 mRNA levels that were increased by low-calcium or low-phosphorus diets and induced hypocalcemia in mice fed a low-calcium diet. Promoter analysis revealed that T3 decreases the basal transcriptional activity of the CYP27B1 gene through thyroid hormone receptors (TRα and TRβ1) and the retinoid X receptor α (RXRα) in renal proximal tubular cells. Interestingly, we identified an everted repeat negative thyroid hormone response element (1α-nTRE) overlapping the sterol regulatory element (1α-SRE) and the TATA-box −50 to −20 base pairs from the human CYP27B1 gene transcription start site. Finally, we established that CYP27B1 gene transcription is positively regulated by SRE-binding proteins and that a T3-bound TRβ1/RXRα heterodimer inhibits SRE-binding protein-1c-induced transcriptional activity through the 1α-nTRE. These results suggest that transcriptional repression of the CYP27B1 gene by T3-bound TRs/RXRα, acting through the 1α-nTRE, results in decreased renal CYP27B1 expression and plasma 1,25(OH)2D levels.

Thyroid hormone dependent nuclear proteins from rat liver

1982 ◽  
Vol 99 (4) ◽  
pp. 567-572
Author(s):  
Angeles Rodriguez-Pena ◽  
Juan Bernal
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Effective Dose ◽  
Rat Liver ◽  
Physiological Role ◽  
Nuclear Proteins ◽  
Single Administration ◽  
Minimum Effective Dose ◽  
Nuclear Level

Abstract. Two nuclear proteins from rat liver were shown to be dependent on thyroid hormones. These proteins were present in the nucleosol or nucleoplasmic fraction, and were extracted from the nuclei with 0.15 m NaCl at pH8. After thyroidectomy, a 120 000-Mr polypeptide decreased in concentration to levels below 10% of normal control rats and another polypeptide of 81 000-Mr was increased. Treatment with T4 at physiological replacement doses for several days restored the levels of both proteins to normal. A single administration of 50 μg T3 induced a detectable increase of 120K after 14 h, with maximal effects at 48 h after administration. The minimum effective dose of T3 on 120K was 0.5 μg administered for three days. Preliminary observations suggest that the response of 81K to thyroid hormones is much more sensitive than that of 120K. The physiological role of these polypeptides is unknown, but they could be involved in the mode of T3 action at the nuclear level.

Sign in / Sign up

Export Citation Format

Share Document