Plasma Thyroid Hormone Levels Research Articles

Association between low-normal thyroid function and advanced liver fibrosis in metabolic dysfunction-associated fatty liver disease patients: a retrospective cohort study.

Recent studies have found that thyroid function may be associated with the occurrence and development of advanced liver fibrosis in patients with metabolic dysfunction-associated fatty liver disease (MAFLD). However, the majority of such research has consisted of cross-sectional studies. This retrospective cohort study aimed to investigate the effect of low-normal thyroid function on advanced liver fibrosis in MAFLD patients over a 5-year period. This retrospective cohort study enrolled 825 outpatients and inpatients with MAFLD who attended the Third Affiliated Hospital of Sun Yat-sen University (Guangzhou, China) between January 2011 and December 2018. Based on plasma thyroid hormone and thyroid-stimulating hormone levels, these patients were divided into two groups, namely a low-normal thyroid function group and a strict-normal thyroid function group. The fibrosis-4 score was used to assess advanced liver fibrosis. A chi-square test was conducted to compare the occurrence of advanced fibrosis between the groups. Among the 825 MAFLD patients, 117 and 708 were defined as having low-normal thyroid function and strict-normal thyroid function, respectively. Follow-up data were available for 767 patients (93.0%) during a 5-year period. Eight (7.5%) MAFLD patients with low-normal thyroid function and 26 (3.9%) with strict-normal thyroid function developed advanced liver fibrosis and the cumulative incidence was not significantly different (P = 0.163). Stratification analysis showed that the lean MAFLD patients (body mass index ≤ 23 kg/m2) with low-normal thyroid function had a higher risk of advanced liver fibrosis than the lean MAFLD patients with strict-normal thyroid function (P < 0.05). Low-normal thyroid function is associated with advanced liver fibrosis among lean MAFLD patients.

Thyroid hormone manipulation influences development of endothermy and hatching in white leghorn chickens (Gallus gallus)

Chickens experience rapid change in their physiology and metabolism during hatching. We propose that thyroid hormones play a major role in regulating the developmental changes associated with attaining endothermy. To better understand the role thyroid hormones play in hatch timing and development of thermogenic capacity and metabolic rate we manipulated plasma thyroid hormone levels in chicken embryos beginning at 80% development (day 17 of a 21-day incubation) with either a single dose of triiodo-L-thyronine (T3) or the thyroperoxidase inhibitor methimazole (MMI). Manipulation of thyroid hormones altered the timing of hatching, accelerating hatching under hyperthyroid conditions, and prolonging hatching with hypothyroid conditions. Effect sizes comparisons of morphological variables between treatment groups revealed larger heart and body masses in hyperthyroid 1-day post hatch animals. Thyroid hormone manipulation influenced the thermal neutral zone for O2 consumption and body temperature during gradual cooling from 35 to 15 °C of externally pipped embryos and 1-day post hatch chicks. Hyperthyroid EP animals had a wider thermal neutral zone during cooling when compared to control animals. At the temperatures tested, the hypothyroid animals did not exhibit a thermal neutral zone. Similar differences between treatments in the breadth of the thermal neutral zone carried through to 1-day post hatch chickens. These findings suggest that thyroid manipulations influence the timing and development of the animal’s thermogenic response to cooling.

Divergent Thyroid Hormone Levels in Plasma and Left Ventricle of the Heart in Compensated and Decompensated Cardiac Hypertrophy Induced by Chronic Adrenergic Stimulation in Mice.

Chronic hemodynamic overload of the heart induces ventricular hypertrophy that may be either compensatory or progress to decompensation and heart failure. The gradual impairment of ventricular function is, at least in part, the result of a reduction of cardiac thyroid-hormone (TH) action. Here, we examined the proposed roles of increased cardiac expression of the TH-inactivating enzyme deiodinase type 3 (D3) and reduced plasma TH levels in diminishing cardiac TH levels. Using minipumps, mice were infused for one and two weeks with isoproterenol (ISO) alone or in combination with phenylephrine (PE). Remodeling of the heart induced by these adrenergic agonists was assessed by echocardiography. Left ventricular (LV) tissue and plasma TH levels (T4 and T3) were determined using liquid chromatography-tandem mass spectrometry. LV D3 activity was determined by conversion of radiolabeled substrate and quantification following HPLC. The results show that ISO induced compensated LV hypertrophy with maintained cardiac output. Plasma levels of T4 and T3 remained normal, but LV hormone levels were reduced by approximately 30% after two weeks, while LV D3 activity was not significantly increased. ISO + PE induced decompensated LV hypertrophy with diminished cardiac output. Plasma levels of T4 and T3 were substantially reduced after one and two weeks, together with a more than 50% reduction of hormone levels in the LV. D3 activity was increased after one week and returned to control levels after two weeks. These data show for the first time that relative to controls, decompensated LV hypertrophy with diminished cardiac output is associated with a greater reduction of cardiac TH levels than compensated hypertrophy with maintained cardiac output. LV D3 activity is unlikely to account for these reductions after two weeks in either condition. Whereas the mechanism of the mild reduction in compensated hypertrophy is unclear, changes in systemic TH homeostasis appear to determine the marked drop in LV TH levels and associated impairment of ventricular function in decompensated hypertrophy.

Plasma T3 and T4 Hormone Levels as Reference Values in Rehabilitated Common Buzzard (Buteo buteo), Long-Legged Buzzard (Buteo rufinus) and Golden Eagle (Aquila chrysaetos)

Applying appropriate criteria for raptors at rehabilitation stages including release and post release determines how healthy the animal can survive in its natural habitat for any length of time. In determining release criteria, clinical examinations of animals as well as clinical data should be evaluated. In this study, plasma T3 and T4 levels of 16 Common Buzzard (Buteo buteo), 7 Long-legged Buzzard (Buteo rufinus) and 7 Golden Eagles (Aquila chrysaetos) were determined at Kafkas University/ Kafkas Wildlife Conservation, Rescue, Rehabilitation Practice and Research Center between 2016-2018. All raptors were kept at the rehabilitation center for 1-3 months in bird care rooms and flight tunnels specially arranged for each species. Rehabilitated birds blood were collected before released to wild. Plasma T3 and T4 hormone levels were analysed and determined in raptors that considered suitable for release. Although small differences were detected between T3 and T4 values as a result of the analysis, no statistical difference was found. These small differences in values may be due to the metabolic responses and environmental conditions of each raptor. As a result, these plasma thyroid hormone levels in rehabilitated raptors can be accepted as reference values.

TOXIC EFFECTS OF AROCLOR 1254 ON RAT HEART AND THYROID AND MODIFYING ROLE OF SELENIUM STATUS

Objective: Polychlorinated biphenyls (PCBs) were very widely used in industrial products in past. These chemicals were banned in the 1970s due to their toxic effects. PCBs can still affect human health, as they are persistent in the environment. Aroclor 1254 (A1254) is a commercial PCB congener which was used in electrical transformers, fluorescent lighting fixtures and old appliances such as televisions or refrigerators. In this study, we aimed to evaluate the toxic effects of A1254 on heart and thyroid in male Sprague-Dawley rats. In addition, the modifying role of selenium status was also evaluated.&#x0D; Material and Method: 8-week-old male Sprague-Dawley (SD) rats were used in the experiment. The animals were separated randomly into 6 groups (n=6) as control; selenium supplemented (SeS); selenium deficient (SeD); A1254 exposed (A); selenium supplemented A1254 exposed (ASeS) and selenium deficient A1254 exposed (ASeD). A1254 was applied by gavage during the last 15 days of feeding period. Heart and thyroid weights and relative weights, plasma thyroid hormone levels, as well as thyroid and heart tissue oxidative/antioxidative parameters were evaluated.&#x0D; Result and Discussion: Results showed that A1254 exposure and selenium deficiency caused oxidative stress on both heart and thyroid. Plasma fT3 and fT4 levels markedly changed in ASeD group. In conclusion, it can be stated that A1254 exposure can cause lead to oxidative/antioxidative imbalance in both thyroid and heart and can disrupt functioning of thyroid hormones. Selenium seems to have a modifying role in A1254 toxicity in both organs, the importance of which should be evaluated with further mechanistic experiments.

Manipulating plasma thyroid hormone levels alters development of endothermy and ventilation in nestling red-winged blackbirds.

Thyroid hormones are key regulators of development and metabolism in vertebrates. During the nestling period, young of altricial species transition from an ectothermic phenotype to an endothermic phenotype. Red-winged blackbirds are an altricial species that exhibit an increase in plasma 3,3', 5-triiodo-L-thyronine (T3) levels during the first 5days post-hatch (dph), begin to develop endothermic metabolic responses by 7 dph, and fledge within 10 days of hatching. We propose that thyroid hormones play an important role in regulating development of endothermy during the nestling period in altricial birds. To better understand the effects of thyroid hormones on endothermic metabolic development in an altricial species, we treated nestling red-winged blackbirds on 2, 3, and 5 dph with either methimazole (MMI) to induce hypothyroidism or supplemental T3 to induce hyperthyroidism. We then measured on 5, 7, and 9 dph morphology and whole animal O2 consumption ( ) and ventilation in the thermal neutral zone and during gradual cooling. Treatment of nestlings with MMI resulted in lower plasma T3 levels on 5 dph that recovered by 7 dph, while supplementing with T3 did not affect plasma T3 levels on 5, 7 and 9 dph. Treatment with MMI resulted in smaller nestlings with smaller hearts and structural characters such as wing chord and femur length, but larger lungs and kidneys. Treatment with T3 produced smaller nestlings with smaller body masses and shorter femur and tarsus lengths. The development of and ventilation endothermic responses to gradual cooling in MMI treated nestlings were delayed when compared with control nestlings. In 9 dph nestlings, hypothyroidism resulted in alterations in the responses of ventilation frequency and tidal volume to cooling when compared with the control nestlings. Supplemental T3 had no effect on the development of and ventilation in the thermal neutral zone or in response to cooling. Our data suggest plasma thyroid hormone levels play an active role in the systemic development of endothermic capacity and the development of ventilatory control. In the nestling avian, multiple systems develop in concert to produce an endothermic phenotype, but reduced thyroid hormone delays maturation of endothermic capacity.

Development and metamorphosis in frogs deficient in the thyroid hormone transporter MCT8

Precisely regulated thyroid hormone (TH) signaling within tissues during frog metamorphosis gives rise to the organism-wide coordination of developmental events among organs required for survival. This TH signaling is controlled by multiple cellular mechanisms, including TH transport across the plasma membrane. A highly specific TH transporter has been identified, namely monocarboxylate transporter 8 (MCT8), which facilitates uptake and efflux of TH and is differentially and dynamically expressed among tissues during metamorphosis. We hypothesized that loss of MCT8 would alter tissue sensitivity to TH and affect the timing of tissue transformation. To address this, we used CRISPR/Cas9 to introduce frameshift mutations inslc16a2, the gene encoding MCT8, inXenopus laevis. We produced homozygous mutant tadpoles with a 29-bp mutation in the l-chromosome and a 20-bp mutation in the S-chromosome. We found that MCT8 mutants survive metamorphosis with normal growth and development of external morphology throughout the larval period. Consistent with this result, the expression of the pituitary hormone regulating TH plasma levels (tshb) was similar among genotypes as was TH response gene expression in brain at metamorphic climax. Further, delayed initiation of limb outgrowth during natural metamorphosis and reduced hindlimb and tail TH sensitivity were not observed in MCT8 mutants. In sum, we did not observe an effect on TH-dependent development in MCT8 mutants, suggesting compensatory TH transport occurs in tadpole tissues, as seen in most tissues in all model organisms examined.

Transplantable human thyroid organoids generated from embryonic stem cells to rescue hypothyroidism

The thyroid gland captures iodide in order to synthesize hormones that act on almost all tissues and are essential for normal growth and metabolism. Low plasma levels of thyroid hormones lead to hypothyroidism, which is one of the most common disorder in humans and is not always satisfactorily treated by lifelong hormone replacement. Therefore, in addition to the lack of in vitro tractable models to study human thyroid development, differentiation and maturation, functional human thyroid organoids could pave the way to explore new therapeutic approaches. Here we report the generation of transplantable thyroid organoids derived from human embryonic stem cells capable of restoring plasma thyroid hormone in athyreotic mice as a proof of concept for future therapeutic development.

Relationship between the development of hyperlipidemia in hypothyroidism patients.

As shown in the previous studies, hypothyroidism (HT) is identified to be closely associated with the elevated plasma levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), triglyceride (TG), and with the decreased plasma levels of high density lipoprotein cholesterol (HDL-C). On the other hand, the thyroid hormone (TH), which has been considered as a vital hormone produced and released by the thyroid gland, are well-established to regulate the metabolism of plasma TC; whereas other evidence proposed that the thyroid-stimulating hormone (TSH) also regulated the plasma cholesterol metabolism independently of the TH, which further promotes the progression of hyperlipidemia. Nevertheless, the potential mechanism is still not illustrated. It is worth noting that several studies has found that the progression of HT-induced hyperlipidemia might be associated with the down-regulated plasma levels of TH and the up-regulated plasma levels of TSH, revealing that HT could promote hyperlipidemia and its related cardio-metabolic disorders. Otherwise, multiple novel identified plasma proteins, such as proprotein convertase subtilisin/kexin type 9 (PCSK9), angiopoietin-like protein (ANGPTLs), and fibroblast growth factors (FGFs), have also been demonstrated to embrace a vital function in modulating the progression of hyperlipidemia induced by HT. In the present comprehensive review, the recent findings which elucidated the association of HT and the progression of hyperlipidemia were summarized. Furthermore, other results which illustrated the underlying mechanisms by which HT facilitates the progression of hyperlipidemia and its cardio-metabolic disorders are also listed in the current review.

Menorrhagia as main presentation sign of severe hypothyroidism in a pediatric patient: a case report

BackgroundThe relative high frequency of menstrual irregularities in the first two–three years after menarche may lead to the risk of underestimation of associated pathological conditions, which are always to be accurately researched with careful examination and anamnesis. The association between menstrual irregularities and hypothyroidism is described in literature but the available data are scarce and mainly based on adult case series. It is described that low plasma levels of thyroid hormone can shift the hemostatic system towards a hypocoagulable and hyperfibrinolytic state and seem to lead to an increased bleeding risk.Case presentationThis case report describes the case of a thirteen years old girl who presented to our Emergency Department complaining of menorrhagia for the last fifteen days, leading to severe anemia. The objective examination revealed clinical signs of hypothyroidism and a severe short stature, lower than mid-parental height, with stunting of growth and a significant bone age delay. Blood exams and thyroid ultrasound were consistent with the diagnosis of severe hypothyroidism in autoimmune thyroiditis with acquired von Willebrand syndrome, growth hormone deficiency. Magnetic resonance showed pituitary functional hyperplasia.The substitutive therapy with levothyroxine led to the resolution of heavy bleeding after five days and following normalization of coagulative parameters and pituitary hyperplasia.ConclusionsHypothyroidism usually presents with unspecific symptoms, with consequent risk of diagnostic delay. It can influence the coagulation system and it seems to be associated to increased risk of menstrual irregularities.We underline the importance of a regular follow up of the pubertal development, including height measurements, thyroid palpation and menstrual anamnesis to intercept red flags findings for hypothyroidism.

The effectiveness of human chorionic gonadotropin in stimulation of second spermiation in pikeperch Sander lucioperca during the spawning season

The aim of the present study was to evaluate the effectiveness of human chorionic gonadotropin (hCG) in stimulation of second spermiation in already reproduced pikeperch males during the same spawning season. Fish (mean weight 919.9 ± 236.9 g) were divided into the control saline-injected group, and two groups injected with 200 and 400 IU hCG/kg body weight. Forty-eight hours following injection (at a temperature of 16.7 °C) the percentage of fish producing useable amounts of semen increased from 30% in the control group up to 80% in the treated fish and the highest volume of semen was recorded in fish treated with 400 IU/kg BW hCG. Spermatocrit (50.7 ± 9.1%) and sperm concentration (17.5 ± 5.0 × 109 spermatozoa/mL) were significantly higher in control fish than those recorded in hCG-treated fish (24.8 ± 7.7% and 8.1 ± 2.4 × 109 spermatozoa/mL in 200 IU/kg; 32.3 ± 17.6% and 10.9 ± 7.5 × 109 spermatozoa/mL in 400 IU/kg). No significant differences were observed between the groups with respect to sperm motility (as a spermatozoa activity time and percentage); however, a change in plasma alkaline phosphatase activity was found in the group injected with 400 IU/kg of hCG. The lack of significant differences in plasma metabolites and cortisol between control and hCG-treated fish indicated that the hCG had no effect on the stress response. Testosterone levels were significantly increased in the hCG-treated fish, whereas no significant differences in 17β-estradiol were recorded. No differences between the groups in plasma levels of thyroid hormones suggested lack of hCG-induced effect on hypothalamus-pituitary-thyroid axis. The results of this study demonstrated that the spermiation of already reproduced pikeperch males could be induced by hCG during the same spawning season. Based on the results on semen volume and concentration, injection with hCG could improve the efficiency of pikeperch reproduction to reduce the number of brooders and costs of juvenile pikeperch production.

Simulation of the plasma level of thyroid hormones for a total thyroidectomized virtual-patient treated by BMI and BSA-based LT4 monotherapy dose regimen

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Thyrotropic effects of balneotherapy in Truskavets’ spa and their endocrine, vegetative and metabolic accompaniments

Background. Previous studies of the Truskavetsian Scientific School of Balneology have studied the effects of course use of bioactive water Naftussya - the main therapeutic factor of the spa - on plasma levels of thyroid hormones in males and females healthy rats and women with thyroid hyperplasia. In men with chronic cholecystitis, the immediate thyrotropic effects of a single use of Naftussya water have been studied. The aim of this study is thyrotropic effects of balneotherapy in Truskavets’ spa and their endocrine, vegetative and metabolic accompaniments in men and women with chronic cholecystitis and pyelonephritis. Materials and Methods. The object of clinical-physiological observation were 34 men (23-70 years) and 10 women (39-76 years), who underwent rehabilitation treatment of chronic cholecystitis and pyelonephritis in remission in the Truskavets’ spa. The examination was performed twice, before and after a 7-10-day course of balneotherapy. The main object of study was the plasma level of Triiodothyronine. We determined also content in plasma Cortisol, Aldosterone, Testosterone and Calcitonin as well as the parameters of the HRV and metabolism. Results. We find in 16 patients (12 men and 4 women) inhibitory thyrotropic effect, in 22 (16 men and 6 women) neutral, and in 6 men only – enhancing effect of balneotherapy. Each variant of the thyrotropic effect is accompanied by characteristic changes in testosteronemia, calcitoninemia, parathyroid activity, Heart Rate, Baevskiy’s Activity Regulatory Systems Index, HRV-markers of vagal tone, Calciemia as well as VLD and LD lipoproteins Cholesterol plasma. Conclusion. Our data confirmed and supplemented the provisions on the multivariate effects of balneotherapy in the spa of Truskavets’ on the endocrine and autonomic nervous systems and metabolism of patients.

MINERAL DENSITY AND PROCESSES OF BONE TISSUE REMODELING IN CHILD POPULATION LIVING IN IODINE-DEFICIENT BIOGEOCHEMICAL TERRITORY

The territory of the Republic of Bashkortostan belongs to the regions with natural iodine deficiency in soil and water. The population of the republic is at risk of developing iodine deficiency conditions. The aim of the study was to evaluate the frequency of a decrease in bone mineral density and the level of markers of osteoresorption and bone formation in young schoolchildren and adolescents living in a region with natural iodine deficiency. Materials and methods. The survey covered 288 students of general education schools aged 11–12 and 309 students aged 14–15. Theauthors studiedconcentration of iodine in urine, plasma levels of thyroid hormones (thyroid stimulating hormone, free thyroxine), levels of calcium, magnesium, phosphorus, C-terminal telopeptides of type I collagen, activity of the bone isoenzyme of alkaline phosphatase. The volume of the thyroid gland, the mineral density of the bone tissue of the middle diaphysis of the tibia, the lower third of the radius were determined by ultrasonometry. Results and discussion. It was found that children have a high prevalence of iodine deficiency from 44% to 57.6% and a decrease in the concentration of iodine in the urine, an increase in the content of thyrotropin, calcium and magnesium in the blood plasma. Insufficient iodine supply leads to a slowdown in the intensity and imbalance of remodeling with a decrease in bone formation processes.

Seasonal Changes in Plasma Hormones, Sex-Related Genes Transcription in Brain, Liver and Ovary during Gonadal Development in Female Rainbow Trout (Oncorhynchus mykiss)

The purpose of this study was to investigate the periodic seasonal changes in endocrine activity and gonadal development of female rainbow trout (Oncorhynchus mykiss) in a high-altitude cold-water environment. The fish were sampled monthly from January to November and the levels of plasma hormones (estradiol (E2), cortisol and thyroid hormones (THS)) and vitellogenin (VTG) were measured by ELISA. Moreover, the transcriptions of sex-related genes in the ovary, brain, and liver were detected by qRT-PCR. The results showed a seasonal fluctuation of plasma hormones and VTG together with the development of the ovary, which reached a peak from August to October. Similarly, the transcription of hypothalamic gonadotropin-releasing hormone-2 (cgnrh-2), hypothalamic gonadotropin-releasing hormone receptors (gnrhr) and follicle-stimulating hormone (fsh) in the brain varied from January to September, but the highest level was detected in September to November. In addition, the transcription of sex-related genes located in the ovary and liver increased significantly during August to October, accompanied by a continuous increase in the gonadosomatic index (GSI) and a decrease in the hepatosomatic index (HSI). Therefore, plasma hormones and sex-related genes regulate the development and maturation of O. mykiss oocytes with the change in seasons and peaked in November. The results of this study provide a reference for improving the efficiency of the artificial reproduction of O. mykiss.

Chrysin restores memory deficit in hypothyroidism mice: Behavioral, neurochemical and computational approaches involving the neurotrophinergic system

Hypothyroidism is a condition that affects multiple systems, including the central nervous system, causing, for example, cognitive deficits closely related to Alzheimer's disease. The flavonoid chrysin is a natural compound associated with neuronal improvement in several experimental models. Here, we evaluated the effect of chrysin on cognitive impairment in hypothyroid female mice by exploring neuroplasticity. Hypothyroidism was induced by continuous exposure to 0.1% methimazole (MTZ) in drinking water for 31 days. On the 32nd day, the animals showed low plasma levels of thyroid hormones (hypothyroid mice) than the control group (euthyroid mice). Subsequently, mice were intragastrically administered with vehicle or chrysin (20 mg/kg) once a day for 28 consecutive days. At the end of the treatments, behavioral tests were performed: open-field test (OFT) and morris water maze (MWM). Then, the levels of neurotrophins (BDNF and NGF) in the hippocampus and prefrontal cortex were measured and tested the affinity of chrysin with neurotrophinergic receptors through molecular docking. Hypothyroid mice showed memory deficit in the MWM and reduced neurotrophins levels in the hippocampus and prefrontal cortex, meanwhile, the chrysin treatment was able to reversed the deficit of spatial memory function and increased the levels of BDNF in hipocamppus and NGF in both structures. Additionally, molecular docking analysis showed that chrysin potentially binds to the active site of the TrkA, TrkB, and p75NTR receptors. Together, these findings suggest that chrysin reversed behavioral and neurochemical alterations associated with memory deficit induced by hypothyroidism, possibly by modulating synaptic plasticity in the neurotrophinergic system.

Effects of oral iodine supplementation in very low birth weight preterm infants for the prevention of thyroid function alterations during the neonatal period: results of a randomised assessor-blinded pilot trial and neurodevelopmental outcomes at 24months.

The trace element iodine (I) is essential for the synthesis of thyroid hormones. Parenteral nutrition solutions, formula milk, and human breast milk contain insufficient iodine to meet recommended intake for preterm infants. Iodine deficiency may affect thyroid function and may be associated with morbidity or neurological outcomes. The primary objective is to assess the evidence that dietary supplementation with iodine affects thyroid function during the neonatal period. The design was a randomised controlled pilot trial. Infants who met the inclusion criteria were enrolled through consecutive sampling and assigned to two different groups. The setting was a Spanish university hospital. Ninety-four patients with very low birth weight (under 1500g) were included. Intervention group: 30µg I/kg/day of iodine in oral drops given to 47 infants from their first day of life until hospital discharge. Control group: 47 infants without supplements. Formula and maternal milk samples for the determination of iodine content were collected at 1, 7, 15, 21, 30days, and at discharge. Blood samples were collected for thyroid hormones. Neurological development was assessed at 2years of age (Bayley III Test). Infants in the supplemented group reached the recommended levels from the first days of life. The researchers detected the effects of iodine balance on the plasma levels of thyroid hormones measured during the first 12weeks of age. The trial assessed the impact of the intervention on neurodevelopmental morbidity.Conclusion: Thyroid function is related to iodine intake in preterm infants. Therefore, supplements should be added if iodine intake is found to be inadequate. The analyses found no effects of iodine supplementation on the composite scores for Bayley-III assessments in all major domains. The study results indicate potentially important effects on language development related to low iodine excretion during the first 4weeks of life What is Known: • Thyroid function is related to iodine intake in preterm infants. • Preterm babies on formula preparations and with exclusive parenteral nutrition are at high risk of iodine deficiency. What is New: • Iodine intake should be monitored during the neonatal period. • Iodine supplements should be added if iodine intake is found to be inadequate.

The Effect of Therapeutic Hypothermia on Plasma Levels of Thyroid Hormones During Hemorrhagic Shock in Adult Male Wistar Rats

Background and Aim: Hemorrhagic shock (HS) is one of the most important causes of death. In this study, we investigated the benefits of therapeutic hypothermia (32°C) during HS on blood pressure (BP) and the role of thyroid hormones during HS. Materials and Methods: Twenty-four male Wistar rats were divided into two normothermic hemorrhagic (NH) and hypothermic hemorrhagic (HH) groups (32°C during shock); the animals were then anesthetized, a microcatheter was inserted into the femoral artery, and one into the femoral vein. The arterial samples were centrifuged, and plasma was isolated to measure thyroid hormones later. The microcatheter was fixed to a physiograph to record BP. Animals were exposed to HS for 90 minutes by withdrawing blood from the femoral vein and BP was assessed during HS. Results: The BP of HH animals was significantly higher in most times of HS and at 40 minutes (56.8±4.2 mmHg) in comparison to NH rats (45.4±3.8 mmHg) (P&lt;0.05). In addition, the amount of BP in HH animals at the end of the shock period at 90 minutes (63.8±5.5 mmHg) was significantly (P&lt;0.001) higher in comparison with the NH groups (39±3.2 mmHg). Levels of thyroid hormones T4 and T3 at the end of shock were lower in the HH group compared to the NH group (P&lt;0.001). Conclusion: Therapeutic hypothermia indirectly reduces the level of thyroid hormones and directly reduces the metabolism of non-vital tissues, preserves blood in the central arteries, and increases BP.

Flame retardants and their associations with thyroid hormone-related variables in northern fulmars from the Faroe Islands

Flame retardants (FRs) are widely reported in tissues of seabirds including birds sampled from remote areas. There is evidence that FRs can disrupt the hypothalamic-pituitary-thyroid (HPT) axis in seabirds, although information is limited on thyroid-related mechanisms and effects. This study investigated the associations between concentrations of polybrominated diphenyl ethers (PBDEs) and other FRs, and changes in the HPT axis in northern fulmars (Fulmarus glacialis) from the Faroe Islands (North Atlantic). Plasma concentrations of thyroid hormones (THs), hepatic deiodinase type 1 (D1) activity, and transcription of selected TH-related genes in liver were used as markers of HPT axis changes. Liver concentrations of a certain PBDE congeners and other FRs including pentabromoethylbenzene (PBEB), dechlorane 602 (Dec-602), and dechlorane plus (DP) were associated with changes in thyroid status. Specifically, liver PBDE, PBEB and Dec-602 concentrations were associated with plasma TH levels (free thyroxine [FT4] and total triiodothyronine [TT3]). Liver DP concentrations were positively correlated with the TT4:FT4 ratios and mRNA levels of UDP-glucuronyltransferase-1, while those of PBEB were negatively associated with TT4:TT3 ratios and D1 activity. D1 activity was also positively associated with the tri-, tetra- and hexa-BDE congeners. Moreover, transcription of ABCC2, a hepatic TH transporter, was associated with certain liver PBDE concentrations. Although PBDEs and other FRs may be potential inhibitors of D1 activity, only a few of the targeted FRs had modest associations with hepatic D1 activity. Regardless, the relationships reported herein indicated that exposure to moderate levels of FRs can be associated with thyroid axis perturbation at the molecular/biochemical levels in this North Atlantic seabird species.

Protein arginine methyltransferase 1 regulates cell proliferation and differentiation in adult mouse adult intestine

BackgroundAdult stem cells play an essential role in adult organ physiology and tissue repair and regeneration. While much has been learnt about the property and function of various adult stem cells, the mechanisms of their development remain poorly understood in mammals. Earlier studies suggest that the formation of adult mouse intestinal stem cells takes place during the first few weeks after birth, the postembryonic period when plasma thyroid hormone (T3) levels are high. Furthermore, deficiency in T3 signaling leads to defects in adult mouse intestine, including reduced cell proliferation in the intestinal crypts, where stem cells reside. Our earlier studies have shown that protein arginine methyltransferase 1 (PRMT1), a T3 receptor coactivator, is highly expressed during intestinal maturation in mouse.MethodsWe have analyzed the expression of PRMT1 by immunohistochemistry and studied the effect of tissue-specific knockout of PRMT1 in the intestinal epithelium.ResultsWe show that PRMT1 is expressed highly in the proliferating transit amplifying cells and crypt base stem cells. By using a conditional knockout mouse line, we have demonstrated that the expression of PRMT1 in the intestinal epithelium is critical for the development of the adult mouse intestine. Specific removal of PRMT1 in the intestinal epithelium results in, surprisingly, more elongated adult intestinal crypts with increased cell proliferation. In addition, epithelial cell migration along the crypt-villus axis and cell death on the villus are also increased. Furthermore, there are increased Goblet cells and reduced Paneth cells in the crypt while the number of crypt base stem cells remains unchanged.ConclusionsOur finding that PRMT1 knockout increases cell proliferation is surprising considering the role of PRMT1 in T3-signaling and the importance of T3 for intestinal development, and suggests that PRMT1 likely regulates pathways in addition to T3-signaling to affect intestinal development and/or homeostasis, thus affecting cell proliferating and epithelial turn over in the adult.