Thyroid Hormone Secretion Research Articles

Cytomegalovirus-mononucleosis-induced thyroiditis in an immunocompetent patient.

Enteroviruses, including coxsackieviruses and Echovirus, are well known pathogens responsible for the development of thyroiditis. We describe the case of a 49-year-old woman with no personal or family history of thyroid disease who presented to the emergency room with a two-week history of daily fevers up to 39°C, a sore throat, occasional palpitations and diaphoresis, decreased appetite and an unintentional 10 kg weight loss over the same time course Physical examination revealed mild tachycardia, an intention tremor and a normal-sized, nontender thyroid gland without palpable nodules. The remainder of the physical examination was unremarkable and without stigmata of Graves’ disease. Her initial blood tests revealed overt thyrotoxicosis, elevated liver enzymes, an elevated C-reactive protein, a negative monospot and a positive CMV IgM antibody. Thyroid sonography revealed areas of hypoechogenicity and relatively low vascularity. Fine-needle biopsy showed a lymphocytic infiltrate. The patient was treated symptomatically with propranolol. On follow-up, the patient became euthyroid, and her liver enzymes normalised. Previous cases of CMV-induced thyroiditis occurred in immunosuppressed patients. This is the first reported case of a CMV-mononucleosis-induced thyroiditis in an immunocompetent adult patient and serves as a reminder that viral illnesses are a common cause of thyroiditis with abnormal liver enzymes.Learning points:The differential diagnosis of thyrotoxicosis with abnormal liver enzymes includes severe hyperthyroidism and thyroid storm caused by Graves’ disease as well as the thyrotoxic phase of a thyroiditis, usually caused by a virus such as coxsackievirus or, in this case, cytomegalovirus.Cytomegalovirus appears to be a recently recognized causal agent for thyroiditis, both in immunosuppressed and immunocompetent patients.Careful follow-up of thyroid function tests in patients with thyroiditis allows clinicians to determine if patients’ thyroid hormone secretion normalizes or if they remain hypothyroid.

Differential Regulation of Thyroid Hormone Metabolism Target Genes during Non-thyroidal [corrected] Illness Syndrome Triggered by Fasting or Sepsis in Adult Mice.

Fasting and sepsis induce profound changes in thyroid hormone (TH) central and peripheral metabolism. These changes affect TH action and are called the non-thyroidal illness syndrome (NTIS). To date, it is still debated whether NTIS represents an adaptive response or a real hypothyroid state at the tissue level. Moreover, even though it has been considered the same syndrome, we hypothesized that fasting and sepsis induce a distinct set of changes in thyroid hormone metabolism. Herein, we aimed to evaluate the central and peripheral expression of genes involved in the transport (MCT8/Slc16a2 and MCT10/Slc16a10), metabolism (Dio1, Dio2, and Dio3) and action (Thra and Thrb) of TH during NTIS induced by fasting or sepsis. Male mice were subjected to a 48 h period of fasting or cecal ligation and puncture (CLP)-induced sepsis. At the peripheral level, fasting led to: (1) reduced serum thyroxine (T4) and triiodothyronine (T3), expression of Dio1, Thra, Slc16a2, and MCT8 protein in liver; (2) increased hepatic Slc16a10 and Dio3 expression; and (3) decreased Slc16a2 and Slc16a10 expressions in the thyroid gland. Fasting resulted in reduction of Tshb expression in the pituitary and increased expression of Dio2 in total hypothalamus, arcuate (ARC) and paraventricular (PVN) nucleus. CLP induced sepsis resulted in reduced: (1) T4 serum levels; (2) Dio1, Slc16a2, Slc16a10, Thra, and Thrb expression in liver as well as Slc16a2 expression in the thyroid gland (3) Thrb and Tshb mRNA expression in the pituitary; (4) total leukocyte counts in the bone marrow while increased its number in peritoneal and pleural fluids. In summary, fasting- or sepsis-driven NTIS promotes changes in the set point of hypothalamus-pituitary-thyroid axis through different mechanisms. Reduced hepatic THRs expression in conjunction with reduced TH transporters expression in the thyroid gland may indicate, respectively, reduction in the peripheral action and in the secretion of TH, which may contribute to the low TH serum levels observed in both models.

Amiodarone-induced thyrotoxicosis: state of the art

В обзоре представлены данные литературы последних лет о патогенезе, диагностике, лечении амиодарон-индуцированного тиреотоксикоза (АИТ), который является частым осложнением терапии амиодароном (Ам). Описаны изменения секреции и метаболизма тиреоидныхгомонов под влиянием кратковременной и длительной терапии Ам. Развитие АИТ всегда приводит к ухудшению течения аритмии, усугублению недостаточности кровообращения, утяжелению состояния пациента. Выделяют АИТ 1 типа и АИТ 2 типа, а также смешанную форму. Описаны диагностические критерии АИТ 1 и 2 типа. Наиболее информативным тестом для дифференциальной диагностики АИТ 1, 2 типов и смешанных форм является сонография щитовидной железы с допплеровским исследованием кровотока и сканирование с 99mTc-sestaMIBI. Тактика лечения определяется типом АИТ, состоянием сердечно-сосудистой системы, риском повторных аритмий. Консервативное лечение зависит от типа АИТ и осуществляется тиреостатиками или глюкокортикоидами. Обсуждается возможность продолжения антиаритмической терапии Ам у пациентов, перенесших АИТ. При АИТ 1 типа и смешанной форме требуется отмена препарата, если это невозможно – радикальное лечение тиреотоксикоза (радиойодтерапия, тиреоидэктомия). АИТ 2 типа является самолимитирующимся процессом, при жизненно угрожающих аритмиях прием Ам может быть продолжен. Показана эффективность радиойодтерапии для радикального лечения тиреотоксикоза при АИТ 1 и 2 типа, несмотря на низкий захват радиойода. Однако этот вопрос требует дальнейшего изучения и обсуждения. Для быстрого восстановления эутиреоза у тяжелых больных применяют плазмаферез и тиреоидэктомию.

EXPLORATION OF GOITROGENIC/ANTITHYROIDAL POTENTIALITY OF BAMBOO-SHOOTS IN RELATION TO THIOUREA

Objective: Natural goitrogens present in plant foods or antithyroidal drugs both alter the morphology and normal functional status of the thyroid gland interfering the synthesis and secretion of thyroid hormones. In this study, the goitrogenic potential of bamboo shoots (BS) containing natural goitrogens has been compared against a potent synthetic antithyroidal drug thiourea.Methods: BS was fed to 6 rats by 1/3rdreplacement of 180grams (g) of their food i.e.60g of BS containing 35g of goitrogens of cyanogenic origin such that each rat ideally consumed 6 mg/100g of body weight per day and thiourea at a near equal dose of 6 mg/100g of body weight per day was force fed to another 6 rats for a period of 45 d. Changes in food consumption pattern, serum toxicity marker SGOT and SGPT, morphological changes like thyroid gland weight and histology and functional aspects like TPO activity, Na+-K+ATPase activity, urinary iodine excretion and serum T3,T4 and TSH levels induced by this natural and synthetic agent respectively were investigated. Results analyzed by ANOVA followed by post hoc tests.Results: Food consumption pattern was similar in all groups while serum toxicity markers SGOT, SGPT showed a non-significant increase in experimental groups. Increase in body and thyroid gland weight as compared to control was seen on treatment with both antithyroidal agents, a greater percentage of increase was seen in thiourea treated group. TPO activity, Na+-K+ATPase activity, serum T3 and T4levels were decreased significantly in both treated groups as compared to normal, with maximum inhibition in the thiourea treated group. Histological plates of BS treated thyroid revealed hypertrophy and thyroid follicular cell disruption with microcytic infiltration. Thiourea treated gland histological plate revealed complete abolition of normal histoarchitecture with marked changes in colloidal area and hyperplasia with folding and papillae on the epithelium.Conclusion: In overall, the data indicate that though the goitrogenic potentiality of BS cannot be considered having similar efficacy to that of thiourea but as a food entity by itself, it has potent antithyroidal activity even in presence of adequate iodine intake.

Recurrent thyrotoxicosis of extrathyroidal origin due to struma ovarii: A case report and review

Struma ovarii (SO) is a recognized, albeit infrequent, cause of ectopic thyroid hormone secretion. Due to its rarity, only a few cases had been reported with fairly detailed information on thyroid function test (TFT) results. Furthermore, data are limited in the extent of local spread, surgical approach, and postoperative management. A 41-year-old woman from Libya presented with tremor, nervousness, weight loss, heat intolerance, and palpitation. She had also complained of lower abdominal pain and delayed periods. Two years earlier, she was diagnosed with hyperthyroidism, treated with a 12-month course of antithyroid medications resulting in full resolution of symptoms. Her TFTs revealed elevated serum triiodothyronine, thyroxine (T4), free T4, and low thyroid-stimulating hormone (TSH). Pelvic ultrasonography showed a left ovarian cystic mass and a suspicious of ectopic pregnancy was suggested. Abdominal surgical exploration with left salpingo-oophorectomy was performed. Gross and microscopic examinations confirmed the diagnosis of SO. Four weeks later, TFTs were repeated and revealed a high level of serum TSH, and low total T4 and free T4 levels. L-thyroxine replacement was started. In conclusion, Determination of the cause of thyrotoxicosis is essential for proper management. If clinical data and initial investigations are not consistent with common causes of hyperthyroidism, whole-body radioactive iodine scan should be considered. The definitive treatment for patients with SO is surgical resection via laparoscopic approach.

Thyroid emergencies : Thyroid storm and myxedema coma

Thyroid emergencies are rare life-threatening endocrine conditions resulting from either decompensated thyrotoxicosis (thyroid storm) or severe thyroid hormone deficiency (myxedema coma). Both conditions develop out of along-standing undiagnosed or untreated hyper- or hypothyroidism, respectively, precipitated by an acute stress-associated event, such as infection, trauma, or surgery. Cardinal features of thyroid storm are myasthenia, cardiovascular symptoms, in particular tachycardia, as well as hyperthermia and central nervous system dysfunction. The diagnosis is made based on clinical criteria only as thyroid hormone measurements do not differentiate between thyroid storm and uncomplicated hyperthyroidism. In addition to critical care measures therapy focusses on inhibition of thyroid hormone synthesis and secretion (antithyroid drugs, perchlorate, Lugol's solution, cholestyramine, thyroidectomy) as well as inhibition of thyroid hormone effects in the periphery (β-blocker, glucocorticoids).Cardinal symptoms of myxedema coma are hypothermia, decreased mental status, and hypoventilation with risk of pneumonia and hyponatremia. The diagnosis is also purely based on clinical criteria as measurements of thyroid hormone levels do not differ between uncomplicated severe hypothyroidism and myxedema coma. In addition to substitution of thyroid hormones and glucocorticoids, therapy focusses on critical care measures to treat hypoventilation and hypercapnia, correction of hyponatremia and hypothermia.Survival of both thyroid emergencies can only be optimized by early diagnosis based on clinical criteria and prompt initiation of multimodal therapy including supportive measures and treatment of the precipitating event.

Iodine excess exposure during pregnancy and lactation impairs maternal thyroid function in rats.

Adequate maternal iodine consumption during pregnancy and lactation guarantees normal thyroid hormones (TH) production, which is crucial to the development of the fetus. Indeed, iodine deficiency is clearly related to maternal hypothyroidism and deleterious effects in the fetal development. Conversely, the effects of iodine excess (IE) consumption on maternal thyroid function are still controversial. Therefore, this study aimed to investigate the impact of IE exposure during pregnancy and lactation periods on maternal hypothalamus–pituitary–thyroid axis. IE-exposed dams presented reduced serum TH concentration and increased serum thyrotropin (TSH) levels. Moreover, maternal IE exposure increased the hypothalamic expression of Trh and the pituitary expression of Trhr, Dio2, Tsha and Tshb mRNA, while reduced the Gh mRNA content. Additionally, IE-exposed dams presented thyroid morphological alterations, increased thyroid oxidative stress and decreased expression of thyroid genes/proteins involved in TH synthesis, secretion and metabolism. Furthermore, Dio1 mRNA expression and D1 activity were reduced in the liver and the kidney of IE-treated animals. Finally, the mRNA expression of Slc5a5 and Slc26a4 were reduced in the mammary gland of IE-exposed rats. The latter results are in accordance with the reduction of prolactin expression and serum levels in IE-treated dams. In summary, our study indicates that the exposure to IE during pregnancy and lactation induces primary hypothyroidism in rat dams and impairs iodide transfer to the milk.

Thyroid Hormone Availability and Action during Brain Development in Rodents.

Thyroid hormones (THs) play an essential role in the development of all vertebrates; in particular adequate TH content is crucial for proper neurodevelopment. TH availability and action in the brain are precisely regulated by several mechanisms, including the secretion of THs by the thyroid gland, the transport of THs to the brain and neural cells, THs activation and inactivation by the metabolic enzymes deiodinases and, in the fetus, transplacental passage of maternal THs. Although these mechanisms have been extensively studied in rats, in the last decade, models of genetically modified mice have been more frequently used to understand the role of the main proteins involved in TH signaling in health and disease. Despite this, there is little knowledge about the mechanisms underlying THs availability in the mouse brain. This mini-review article gathers information from findings in rats, and the latest findings in mice regarding the ontogeny of TH action and the sources of THs to the brain, with special focus on neurodevelopmental stages. Unraveling TH economy and action in the mouse brain may help to better understand the physiology and pathophysiology of TH signaling in brain and may contribute to addressing the neurological alterations due to hypo and hyperthyroidism and TH resistance syndromes.

Penatalaksanaan Pasien Krisis Tiroid di Intensive Care Unit

Thyroid storm is an emergency in the field of endocrine with high morbidity and mortality. Early diagnosis and proper management will give a good prognosis. Diagnosis of thyroid storm based on the clinical picture of patient, not the laboratory findings. High fever, accompanied by disorders of the central nervous system, cardiovascular system and digestive system are the typical symptoms and signs. Thyroid storm occurs frequently in patients with hyperthyroidism that received inadequate therapy and triggered by infection, trauma, thyroid surgery, or uncontrolled diabetes mellitus. In this case report we present a 36 years old female admitted at emergency unit with a history of Graves’ disease. She presented with loss of consciousness, high fever, palpitation, nausea, vomiting, and abdominal pain. Assessment of Burch and Wartofsky revealed a score of 90. The patient is managed aggressively in ICU. Management of thyroid storm include decreasing the synthesis and secretion of thyroid hormones, lowering peripheral influence of thyroid hormones, preventing systemic decompensation, and treatment of triggering disease when emergency state has been resolved.

Modulation of Calcitonin, Parathyroid Hormone, and Thyroid Hormone Secretion by Electrical Stimulation of Sympathetic and Parasympathetic Nerves in Anesthetized Rats.

The thyroid and parathyroid glands are dually innervated by sympathetic (cervical sympathetic trunk [CST]) and parasympathetic (superior laryngeal nerve [SLN]) nerve fibers. We examined the effects of electrical stimulation of efferent or afferent nerve fibers innervating the thyroid and parathyroid glands on the secretion of immunoreactive calcitonin (iCT), parathyroid hormone (iPTH), 3,3′,5-triiodothyronine (iT3), and thyroxine (iT4) from the thyroid and parathyroid glands. In anesthetized and artificially ventilated rats, thyroid venous blood was collected. The rate of hormone secretion from the glands was calculated from plasma hormone levels, measured by ELISA, and the flow rate of thyroid venous plasma. SLNs or CSTs were stimulated bilaterally with rectangular pulses with a 0.5-ms width. To define the role of unmyelinated nerve fibers (typically efferent), the cut peripheral segments were stimulated at various frequencies (up to 40 Hz) with a supramaximal intensity to excite all nerve fibers. The secretion of iCT, iT3, and iT4 increased during SLN stimulation and decreased during CST stimulation. iPTH secretion increased during CST stimulation, but was not affected by SLN stimulation. To examine the effects of selective stimulation of myelinated nerve fibers (typically afferent) in the SLN, intact SLNs were stimulated with a subthreshold intensity for unmyelinated nerve fibers. iCT, iT3, and iT4 secretion increased during stimulation of intact SLNs at 40 Hz. These results suggest that excitation of myelinated afferents induced by low intensity and high frequency stimulation of intact SLNs promotes secretion of CT and thyroid hormones from the thyroid gland, potentially via reflex activation of parasympathetic efferent nerve fibers in the SLN.

Congenital Secondary Hypothyroidism Evidences in a Dog

Background: Deficiency of thyroid hormones thyroxine (T4) and triiodothyronine (T3) results in multisystemic disease described as hypothyroidism (HpoT). Secondary HpoT is defined by TSH decreased production and, therefore, thyroid hormones. This condition is rare in dogs, accounting for less than 5% of cases. The objective of this report is to describe evidence of congenital secondary hypothyroidism in a mongrel dog and therapeutic response obtained.Case: A 3-year-old neutered male mongrel dog was brought to the veterinarian with a history of overweight without polyphagia, associated with discrete alopecia, poor quality skin and hair coat, lethargy and evident exercise intolerance. Physical examination revealed a body condition score of seven (1 to 9 scale), disqueratosis, pyoderma, ventral cervical alopecia, hair thinning on the posterior surface of the pelvic limbs and nonpalpable thyroid. A body conformation characterized by disproportionate dwarfism was observed. Owners provided a former patient´s X-ray (18 months of age), showing growth plate non-closure in vertebral bodies. Results of a complete blood count (CBC) and serum biochemical profile were within normal limits except for elevated fructosamine (459 µmol/L; reference range: 170-338 µmol/L) and total cholesterol (558 mg/dL; reference range: 135-270 mg/dL). Analyses of the hormone profile showed decreased levels of canine thyroid-stimulating hormone (cTSH) 0.03 ng/mL (reference range: 0.05-0.5 ng/mL), free thyroxine by equilibrium dialysis (fdT4) 0.57 ng/dL (reference range: 0.8-3.0 ng/dL), and total thyroxine (tT4) 5.1 ng/mL (reference range: 15-30 ng/mL). A distal forelimb X-ray was performed and showed opened epiphyseal growth plates from radius and ulnar bones. The patient was discharged with sodium levothyroxine (20 µg/kg PO q 24 hr) until re-evaluation. The patient was re-evaluated 2 months later and clinical symptoms observed at the first admission were still persistent. CBC and serum biochemical profile were within normal range. The values of T4t and cTSH were 21.3 ng/mL (reference range for treated dogs 25-45 ng/mL post-thyroxine) and 0.03 ng/mL respectively. Owners were administering a generic levothyroxine, and then a commercial sodium levothyroxine was prescribed at the same dose for treatment. Clinical improvement was reported by the owner 4 weeks later. A new forelimb and vertebral radiographic examination performed 6 months later revealed complete epiphyseal ossification.Discussion: The patient was diagnosed with central hypothyroidism based on the clinical presentation in conjunction with the laboratory tests results. The main hypothesis argues for a congenital pituitary malformation, leading to a defective hypothalamic-pituitary-thyroid axis function. This decreased hormonal TSH secretion culminated in a chronic mild state of hypothyroidism associated with reduction in the thyroid hormones secretion. Metabolic consequences of mild hypothyroidism affect bone development directly and lead to delayed epiphyseal ossification and epiphyseal growth, reduced long bone growth, and disproportionate dwarfism. Studies have suggested a genetic relation with the development of congenital hypothyroidism, although no disease-causing mutations were found in the genes previously investigated. The prognosis for dogs with secondary hypothyroidism due to malformation or destruction of the pituitary ranges from poor to reserved, with shorter life expectancy in dogs with congenital pituitary malformation due to cysts expansion. Although cost is limiting for some owners, advanced imaging such as computed tomography or magnetic resonance may be useful in the macroscopic evaluation of the pituitary gland and are recommended in central hypothyroidism cases.

Frequency and Spectrum of Chromosomal Aberrations, Acrocentric Chromosome Associations Among Long Livers with Arterial Hypertension and Osteoarthritis Residing in the Carpathian Region

To maintain thyroid homeostasis, a key role is played not only by the adequate provision of a body with iodine, but also with other essential micronutrients, iron in particular. Iron is involved in the conversion of the amino acid L-phenylalanine into L-tyrosine, which is the part of active center of thyroid peroxidase which catalyzes the reactions of oxidation and organification of iodine during the biosynthesis of thyroid hormones. At the same time, insufficient secretion of thyroid hormones leads to mucinous edema of the gastric mucosa and closure of its ductless glands and reduction in both gastric juice secretion and iron absorption. 
 The objective of the research was to determine the influence of latent iron deficiency onto the thyroid status of schoolchildren. 
 Materials and methods. The study involved 68 boys and 65 girls at the age 6-11 years (Group I) and 12-18 years (Group II). To assess iron metabolism, the levels of hemoglobin in capillary blood, serum iron and ferritin, serum iron binding capacity were determined. To clarify the thyroid status in blood serum samples, there were determined the content of free triiodothyronine and thyroxine, thyroid-stimulating hormone of adenohypophysis, urinary iodine concentration; the dimension of the thyroid gland was determined and evaluated considering gender as well as body surface area according to the standards of thyroid volume (97 percentile). 
 Results. It was established that latent iron deficiency can cause thyroid homeostasis disorders, as indicated by the growth of TSH in blood serum of girls by 37.5% (p<0.01) as compared to the control data. The probability of the formation of thyroid dysfunction significantly increases in case of combined iodine and iron deficiency. The development of subclinical hypothyroidism was established in 90.0% of boys and 89.0% of girls at the age of 6-11 years and 100.0% of boys and 75.0% of girls at the age of 12-18 years with mild iodine deficiency and latent iron deficiency. In schoolchildren with microelementosis, an increase in the thyroid gland was revealed in 66.6% of boys and 75.0% of girls of Group I and in half of boys and girls of Group II.
 Conclusions. Iron deficiency can cause changes in thyroid homeostasis even at the stage of preclinical disorders. Latent iron deficiency potentiates the development of subclinical hypothyroidism in case of mild iodine deficiency.

Central hypothyroidism - a neglected thyroid disorder.

Central hypothyroidism is a rare and heterogeneous disorder that is characterized by a defect in thyroid hormone secretion in an otherwise normal thyroid gland due to insufficient stimulation by TSH. The disease results from the abnormal function of the pituitary gland, the hypothalamus, or both. Moreover, central hypothyroidism can be isolated or combined with other pituitary hormone deficiencies, which are mostly acquired and are rarely congenital. The clinical manifestations of central hypothyroidism are usually milder than those observed in primary hypothyroidism. Obtaining a positive diagnosis for central hypothyroidism can be difficult from both a clinical and a biochemical perspective. The diagnosis of central hypothyroidism is based on low circulating levels of free T4 in the presence of low to normal TSH concentrations. The correct diagnosis of both acquired (also termed sporadic) and congenital (also termed genetic) central hypothyroidism can be hindered by methodological interference in free T4 or TSH measurements; routine utilization of total T4 or T3 measurements; concurrent systemic illness that is characterized by low levels of free T4 and normal TSH concentrations; the use of the sole TSH-reflex strategy, which is the measurement of the sole level of TSH, without free T4, if levels of TSH are in the normal range; and the diagnosis of congenital hypothyroidism based on TSH analysis without the concomitant measurement of serum levels of T4. In this Review, we discuss current knowledge of the causes of central hypothyroidism, emphasizing possible pitfalls in the diagnosis and treatment of this disorder.

Do migrant and resident species differ in the timing of increases in reproductive and thyroid hormone secretion and body mass? A case study in the comparison of pre-breeding physiological rhythms in the Eurasian Skylark and Asian Short-toed Lark

BackgroundPhysiological preparation for reproduction in small passerines involves the increased secretion of reproductive hormones, elevation of the metabolic rate and energy storage, all of which are essential for reproduction. However, it is unclear whether the timing of the physiological processes involved is the same in resident and migrant species that breed in the same area. To answer this question, we compared temporal variation in the plasma concentration of luteinizing hormone (LH), testosterone (T), estradiol (E2), triiothyronine (T3) and body mass, between a migrant species, the Eurasian Skylark (Alauda arvensis) and a resident species, the Asian Short-toed Lark (Calandrella cheleensis), both of which breed in northeastern Inner Mongolia, China, during the 2014 and 2015 breeding seasons.MethodsTwenty adult Eurasian Skylarks and twenty Asian Short-toed Larks were captured on March 15, 2014 and 2015 and housed in out-door aviaries. Plasma LH, T (males), E2 (females), T3 and the body mass of each bird were measured every six days from March 25 to May 6.ResultsWith the exception of T, which peaked earlier in the Asian Short-toed Lark in 2014, plasma concentrations of LH, T, E2 andT3 of both species peaked at almost the same time. However, Asian Short-toed Larks attained peak body mass earlier than Eurasian Skylarks. Plasma T3 concentrations peaked 12 days earlier than plasma LH in both species. Generally, plasma LH, T, E2, T3 and body mass, peaked earlier in both species in 2014 than 2015.ConclusionsThe timing of pre-reproductive changes in the endocrine system and energy metabolism can be the same in migrant and resident species; however, residents may accumulate energy reserves faster than migrants. Although migration does not affect the timing of pre-breeding reproductive and metabolic changes, migrant species may need more time to increase their body mass. T levels in resident species may be accelerated by higher spring temperatures that may also advance the pre-breeding preparation of both migrants and residents.

Hypophysectomy abolishes rhythms in rat thyroid hormones but not in the thyroid clock

The endocrine body rhythms including the hypothalamic–pituitary–thyroid axis seem to be regulated by the circadian timing system, and daily rhythmicity of circulating thyroid-stimulating hormone (TSH) is well established. The circadian rhythms are generated by endogenous clocks in the central brain oscillator located in the hypothalamic suprachiasmatic nucleus (SCN) as well as multiple peripheral clocks, but information on the existence and function of a thyroid clock is limited. The molecular machinery in all clock cells is composed of a number of clock genes and their gene products are connected by autoregulatory feedback loops. Here, we provide evidence for a thyroid clock in the rat by demonstrating 24-h antiphase oscillations for the mRNA of the canonical clock genes Per1 and Bmal1, which was unaffected by hypophysectomy. By immunostaining, we supported the existence of a core oscillator in the individual thyroid cells by demonstrating a daily cytoplasmatic–nuclear shuttling of PER1 protein. In normal rats, we found a significant daily rhythmicity in the circulating thyroid hormones preceded by a peak in TSH. In hypophysectomised rats, although the thyroid clock was not affected, the oscillations in circulating thyroid hormones were abolished and the levels were markedly lowered. No daily oscillations in the expression of TSH receptor mRNA were observed in neither control rats nor hypophysectomised rats. Our findings indicate that the daily rhythm of thyroid hormone secretion is governed by SCN signalling via the rhythmic TSH secretion rather than by the local thyroid clock, which was still ticking after hypophysectomy.

Thyroid Hormone Regulation and Insulin Resistance: Insights From Animals Naturally Adapted to Fasting.

The contribution of thyroidal status in insulin signaling and glucose homeostasis has been implicated as a potential pathophysiological factor in humans, but the specific mechanisms remain largely elusive. Fasting induces changes in both thyroid hormone secretion and insulin signaling. Here, we explore how mammals that undergo natural, prolonged bouts of fasting provide unique insight into evolved physiological adaptations that allow them to tolerate such conditions despite intermittent states of reversible insulin resistance. Such insights from nature may provide clues to better understand the basis of thyroidal involvement in insulin dysregulation in humans.

Thyroid hormone status in children with protein energy malnutrition a hospital based case control study

Background: WHO estimates that about half of all deaths, occurring among children aged less than five years in the developing countries, can be attributed to malnutrition. In malnourished children various endocrinal changes are noted. There is reduced synthesis of plasma proteins that affects secretion and metabolism of thyroid hormone. The present study has been conducted to study the effect of protein energy malnutrition (PEM) on thyroid hormone and plasma protein levels; and to find correlation between thyroid hormones and plasma protein levels in PEM children.Methods: A cross sectional hospital based case-control study was carried out in tertiary care hospital of Northern India. 50 children with PEM, and equal number of age and sex matched healthy controls (1-5 years) were included in the study. Detailed clinical assessment of nutritional status followed by anthropometric measurement was recorded in a predesigned performa. The cases were categorized into moderate and severe malnutrition as per WHO classification (weight for height). Free Triiodothyronine (fT3), free Thyroxine (fT4), thyroid stimulating hormone (TSH), serum total protein and serum albumin were estimated. The parameters were compared among cases and controls using appropriate statistical tool. Results: Mean hemoglobin, serum protein, serum albumin, fT3, fT4 and TSH levels were significantly low in case group, when compared to the control group (p <0.001).The levels of biochemical variables, decreases as the severity of malnutrition increases. The difference within the cases (moderate and severe malnutrition) was also found to be statistically significant (p <0.001).Conclusions: PEM is associated with decrease level of thyroid hormone levels and were positively correlated with serum total protein and albumin levels. The decrease level of thyroid hormone may have a contributory role in retarded growth and development.

Optimized FPGA Implementation of the Thyroid Hormone Secretion Mechanism Using CAD Tools.

The goal of this paper is to implement the secretion mechanism of the Thyroid Hormone (TH) based on bio-mathematical differential eqs. (DE) on an FPGA chip. Hardware Descriptive Language (HDL) is used to develop a behavioral model of the mechanism derived from the DE. The Thyroid Hormone secretion mechanism is simulated with the interaction of the related stimulating and inhibiting hormones. Synthesis of the simulation is done with the aid of CAD tools and downloaded on a Field Programmable Gate Arrays (FPGAs) Chip. The chip output shows identical behavior to that of the designed algorithm through simulation. It is concluded that the chip mimics the Thyroid Hormone secretion mechanism. The chip, operating in real-time, is computer-independent stand-alone system.

Generation of Functional Thyroid Tissue Using 3D-Based Culture of Embryonic Stem Cells.

During the last decade three-dimensional (3D) cultures of pluripotent stem cells have been intensively used to understand morphogenesis and molecular signaling important for the embryonic development of many tissues. In addition, pluripotent stem cells have been shown to be a valid tool for the in vitro modeling of several congenital or chronic human diseases, opening new possibilities to study their physiopathology without using animal models. Even more interestingly, 3D culture has proved to be a powerful and versatile tool to successfully generate functional tissues ex vivo. Using similar approaches, we here describe a protocol for the generation of functional thyroid tissue using mouse embryonic stem cells and give all the details and references for its characterization and analysis both in vitro and in vivo. This model is a valid approach to study the expression and the function of genes involved in the correct morphogenesis of thyroid gland, to elucidate the mechanisms of production and secretion of thyroid hormones and to test anti-thyroid drugs.

Aerobic physical exercise in the third trimester in pregnant woman with Hashimoto`s thyroiditis: A case report

Introduction. Physical exercise and thyroid function affect the course and outcome of pregnancy. Pregnancy conversely has an effect on exercise and the secretion of thyroid hormones. It is recommended that pregnant women without medical or obstetric complications engage in physical exercise, as correct exercise and suitable hormonal therapy reduce the risk of a negative course and outcome of the pregnancy. Case report. A 33- year-old marathon runner with diagnosed Hashimoto?s thyroiditis continued to run until she was ready to give birth. The recorded parameters were body mass, and scope and intensity of running. In the third trimester, additional recorded parameters were blood pressure, pulse, blood glucose, prolactin, cortisol and thyroid hormones [thyroxine (T4 and thyroid-stimulating hormone (TSH)]. Foetus growth and development, as well as the status of the subject?s health, were monitored at regular endocrinological and gynaecological examinations. There was an expected increase in body mass during pregnancy, which resulted in a reduction in the running distance and intensity. TSH, cortisol and prolactin blood levels were increased. Statistically, significant correlation has been obtained between TSH and the intensity of running (r = 0.864; p = 0.027). Using the method of cardiotocography (CTG), the average pulse rate in the lower reference range has been recorded (118 bpm). The delivery was induced at the scheduled date. There were no complications in the course and outcome of the pregnancy. Conclusion. Moderate to light aerobic physical exercise had no negative effect on the course and the outcome of the pregnancy in the subject with Hashimoto?s thyroiditis.