Thyroid Hormone Function Research Articles

Hormonal regulation of the phenotype into environmentally appropriate pace‐of‐life syndromes

AbstractThe risk of predation is an important driver that tailors life histories in various ways. Using an evolutionary model based on hormonal control, we study how different predation regimes affect adaptive risk‐taking and growth in fish populations. Growth, metabolism and foraging in the modelled fish are regulated by three simplified hormone functions: growth hormone, orexin, and thyroid hormone. A dynamic state‐dependent optimization model finds optimal hormone profiles for adaptive growth strategies in juvenile fish. We consider a gradient from species where behaviour and metabolic activity have large consequences for risk (typically benthic and camouflaged species), to the opposite endpoint where behaviour may modify predation risk to a smaller degree (as in the pelagic). Along this gradient, the model predicts changes in the pace of life from slow to fast, enacted by up‐regulation of the three hormone functions which in turn increase foraging and metabolism and change the priorities of energy reserves versus growth. Under all types of predation risk investigated, growth is faster when food availability is higher. Energy reserves are maintained primarily during periods of poor food availability and are used to accelerate growth during periods when food availability is high. The thyroid hormone function is up‐regulated predominantly when food availability is high and has an important role in trade‐offs balancing energetic gain and survival. At the individual time scale, the hormone system improves organismic flexibility and robustness. Over the phylogenetic time scale, hormone system adaptations have also restricted the phenotypic plasticity of individuals.

Low T3 Syndrome is Associated with Imbalance of Bone Turnover Biomarker in Patients with Type 2 Diabetes.

To investigate the variation in bone turnover biomarkers among patients with type 2 diabetes (T2D) and low triiodothyronine levels (Low T3 syndrome). This retrospective analytic study included 418 inpatient records from Shanghai Pudong Hospital covering the years 2021 to 2023. Laboratory data related to metabolic and bone turnover biomarkers in patients were analyzed with T2D and the low T3 syndrome. The results indicated that patients with reduced serum T3 levels exhibited statistically significant variations in thyroid function, age, fasting plasma glucose (FPG), glycated hemoglobin A1c (HbA1c), and the proportion of medication history associated with diabetes in comparison to euthyroid patients. In addition to parathyroid hormones, bone turnover biomarkers including N-terminal middle molecular fragment of osteocalcin (NMID), plasma calcium (Ca2+), β C-terminal cross-linking telopeptide of type 1 collagen (β-CTX), and 25-hydroxyvitamin D3 (25 OH VitD3) exhibited significant changes in patients with decreased T3 levels. Evident irregularities were observed in patients with a decreased T3 level, including elevated serum creatinine (SCr), decreased concentrations of albumin and total protein, and a decreased estimated glomerular filtration rate (eGFR), as assessed through hepatic and renal testing, respectively. Significant associations between bone turnover biomarkers and the subsequent variables (gender, adiposity, hepatic, renal, and thyroid function) were revealed through the correlational analysis. Further investigation utilized multivariate linear regression to determine that, in addition to thyroid function, several other factors such as age, gender, bodyweight, pancreatic, hepatic, and renal function, affected the variability in bone turnover biomarkers among patients demonstrating a low serum T3 level. This comparative study demonstrated that despite age, gender, bodyweight, hepatic, renal function, thyroid hormone and pancreatic function were significant factors associated with bone metabolism in patients with T2D and Low T3 syndrome, which may increase the risk of osteoporosis.

Functions and Mechanism of Thyroid Hormone Receptor Action During Amphibian Development.

Thyroid hormones and their receptors (TRs) play critical roles during vertebrate development. One of the most dramatic developmental processes regulated by thyroid hormones is frog metamorphosis, which mimics the postembryonic (perinatal) period in mammals. Here, we review some of the findings on the developmental functions of thyroid hormones and TRs as well as their associated mechanisms of action obtained from this model system. More than 2 decades ago, a dual function model was proposed for TR in anuran development. During larval development, unliganded receptors recruit corepressors to repress thyroid hormone response genes to prevent premature metamorphic changes. Subsequently, when thyroid hormone levels rise, liganded receptors recruit coactivators to activate thyroid hormone response genes, leading to metamorphic changes. Over the years, molecular and genetic approaches have provided strong support for this model and have shown that it is applicable to mammalian development as well as to understanding the diverse effects of thyroid hormones in normal physiology and diseases caused by thyroid hormone signaling dysfunction.

A COMPREHENSIVE REVIEW OF AGNI AND ITS ROLE IN THE ETIOPATHO-GENESIS OF THYROID DYSFUNCTION: A HIGHLY WIDESPREAD DISEASE

Ayurveda is an alternative medicine system that originated in the Indian subcontinent. Ayurveda believes that the universe is made up of five elements: Vayu (air), Jala (water), Aakash (space or ether), Prithvi (earth), and Teja (fire). Ayurveda emphasises the maintenance and promotion of health and the prevention of diseases through various dietary and lifestyle regimens and the treatment of diseases through various therapeutic measures, substantiating the principle “Swasthasya Swasthya Rakshanam,” i.e., preserving the health of healthy persons, and “Aturashya Vikar Prasamanam,” i.e., curing the diseases of the diseased. Sushruta has described the features of a healthy person, i.e., doshas must be in equilibrium, the digestive fire (Agni) must be in a balanced state, and the tissues (Dhatus) and Malas (wastes) must work in a normal state. Agni regulates numerous metabolic reactions, including digestion and cell growth. It is related to a stance or entity that brings about transformation in any form. It supports healthy digestion, joy, and happiness and preserves body tempera-ture and complexity. Thyroid hormones play a crucial part in maintaining homeostasis in the body and function in food digestion at the GI level, which assists in biochemical reactions at the tissue level and helps convert het-erogeneous chemicals to homogeneous ones. An imbalance in Thyroid hormones plays a crucial role in metabol-ic processes. Thyroid hormone functioning can be normal or disordered, similar to Agni in Ayurveda. Agni leads to various metabolic disorders like thyroid disorders. So here, an attempt is made to address the essential func-tions of thyroid hormones as a part of Agni.

The Effects of Triiodothyronine on the Free Thyroxine Set Point Position in the Hypothalamus Pituitary Thyroid Axis.

In clinical endocrinology, it is often assumed that the results of thyroid hormone function tests (TFTs) before total thyroidectomy are considered euthyroid when the circulating concentrations of thyrotropin [TSH] and free thyroxine [FT4] are within the normal reference ranges. Postoperative thyroid replacement therapy with levothyroxine. The aim of L-T4 is to reproduce the preoperative euthyroid condition. Currently, intra-individual changes in the euthyroid set point before and after total thyroidectomy are only partly understood. After total thyroidectomy, a greater postoperative [FT4] than preoperative [FT4] for equivalent euthyroid [TSH] was found, with differences ranging from 3 to 8 pmol/L. This unexplained difference can be explained by the use of a mathematical model of the hypothalamus-pituitary-thyroid (HPT) axis set point theory. In this article, the postoperative HPT euthyroid set point was calculated using a dataset of total thyroidectomized patients with at least three distinguishable postoperative TFTs. The postoperative [TSH] set point was used as a homeostatic reference for the comparison of preoperative TFTs. The preoperative [FT4] value was equal to the postoperative [FT4] value in 50% of the patients, divided by a factor of ~ 1.25 (within +/- 10%). The factor of 1.25 stems from the lack of postoperative use of thyroidal triiodothyronine (T3). Furthermore, approximately 25% of the patients presented a greater preoperative [FT4] difference than postoperative [FT4]/1.25 combined with a normal [TSH] difference. Based on these observations, the effect of T3 on the value of the [FT4] set point was analyzed and explained from a control theory perspective.

Investigation of the thyroid function in end-stage renal failure disease in a Baquba teaching hospital/Diyala governorate - Iraq

Renal failure is the inability of the kidneys to excrete nitrogenous waste products, resulting in their retention in the bloodstream. Several correlations exist between renal and thyroid functions; however, end-stage renal failure is unlikely to be influenced by thyroid hormone function and is connected to a higher prevalence of hypothyroidism. The purpose of this study is to ascertain how thyroid status and renal function relate to renal failure patients. Serum creatinine and urea levels were tested in 50 healthy persons and 100 patients with renal failure illness. The acquired data showed that, in comparison to the control group, the average levels of creatinine and urea were significantly higher. The sick group recorded (122.98 mg/dL and 6.55 mg/dL) and (28.38 mg/dL and 0.75 mg/dL) in comparison to the control group, which has urea and creatinine values within the virtually normal range, respectively. In contrast, TSH levels showed no significant differences and have values within the normal range of TSH values, with 2.33 mIU/L for the experimental group and 2.0 mIU/L for the control group. In contrast, T4 values of the experimental group showed significantly lower levels than the control group, with 83.42 ng/dL compared to 103.77 ng/dL. T3 values, however, showed no significant changes and remained within the normal range of 1.75 to 1.64 nmol/L. In addition, the results demonstrated significant differences in the mean levels of anti-TPO, anti-Tg, and anti-TSHR antibodies. The anti-Tg showed a significant decrease in mean values, which were 28.89 IU/ml and 79.49 IU/ml compared to the control group ranges of 34.41 and 86.68 IU/mL. Finally, anti-TSHR showed a significant increase in the mean, which was 1.24 IU/L compared to 1.18 IU/L in the control group.

Thyroid disrupting effects and the developmental toxicity of hexafluoropropylene oxide oligomer acids in zebrafish during early development

As perfluorooctanoic acid (PFOA) alternatives, hexafluoropropylene oxide dimeric acid (HFPO-DA) and hexafluoropropylene oxide trimeric acid (HFPO-TA) have been increasingly used and caused considerable water pollution. However, their toxicities to aquatic organisms are still not well known. Therefore, in this study, zebrafish embryos were exposed to PFOA (0, 1.5, 3 and 6 mg/L), HFPO-DA (0, 3, 6 and 12 mg/L) and HFPO-TA (0, 1, 2 and 4 mg/L) to comparatively investigate their thyroid disrupting effects and the developmental toxicity. Results demonstrated that waterborne exposure to PFOA and its two alternatives decreased T4 contents, the heart rate and swirl-escape rate of zebrafish embryos/larvae. The transcription levels of genes related to thyroid hormone regulation (crh), biosynthesis (tpo and tg), function (trα and trβ), transport (transthyretin, ttr), and metabolism (dio1, dio2 and ugt1ab), were differently altered after the exposures, which induced the thyroid disrupting effects and decreased the heart rate. In addition, the transcription levels of some genes related to the nervous system development were also significantly affected, which was associated with the thyroid disrupting effects and consequently affected the locomotor activity of zebrafish. Therefore, HFPO-DA and HFPO-TA could not be safe alternatives to PFOA. Further studies to uncover the underlying mechanisms of these adverse effects are warranted.

Phenylbutyrate Treatment in a Boy with MCT8 Deficiency: Improvement of Thyroid Function Tests and Possible Livertoxicity.

Monocarboxylate transporter 8 (MCT8) deficiency is a rare X-chromosomal inherited disease leading to severe cognitive impairment, muscular hypotonia and symptoms of peripheral thyrotoxicosis. Experimental approaches aiming to functionally rescue mutant MCT8 activity by the chemical chaperone phenylbutyrate (PB) demonstrated promising effects in vitro for several MCT8 missense mutations. The objective was to evaluate biochemical and clinical effects of PB in doses equivalent to those approved for the treatment of urea cycle disorders in a boy with MCT8 deficiency due to a novel MCT8 missense mutation c.703G > T (p.V235L). During a treatment period of 13 months, PB led to a significant decrease of elevated TSH and T3 serum concentrations, while fT4 increased. Weight z-score of the toddler remained remarkably stable during the treatment period. Neurodevelopmental assessments (BSID-III) revealed a slight increase of gross motor skills from developmental age 4 to 6 months. However, increasing liver enzyme serum activities and accumulation of phenylacetate (PAA) in urine led to treatment interruptions and dose alterations. In vitro analyses in MDCK1 cells confirmed the pathogenicity of MCT8 p.V235L. However, while PB increased expression of the mutant protein, it did not rescue T3 transport, suggesting a PB effect on thyroid function tests independent of restoring MCT8 activity. In a clinical attempt of PB treatment in MCT8 deficiency we observed a significant improvement of thyroid hormone function tests, tendencies towards body weight stabilization and slight neurodevelopmental improvement. Hepatotoxicity of PB may be a limiting factor in MCT8 deficiency and requires further investigation.

Synergistic Therapy for Graves’ Ophthalmopathy-Associated Eyelid Retraction: Steroid, 5-FU, and Botulinum Neurotoxin a Combination

Background: Graves’ ophthalmopathy (GO) is characterized by upper eyelid retraction (UER), the most prevalent clinical sign. We aimed to assess the clinical efficacy of a multimodal combination of steroids, 5-fluorouracil (5-FU), and botulinum neurotoxin A (BoNT-A) injections in managing UER with GO and analyze the clinical factors in relation to the injection response. Methods: A total of 37 eyes from 23 patients were enrolled for UER with GO. At the endocrinology clinic, the patients were referred to the ophthalmology clinic after taking antithyroid medication for an average of 5.76 months (13 patients), while 10 patients were initially diagnosed with GO and referred to the endocrinology clinic for management of the thyroid hormone function. They performed an orbital computed tomography (CT) scan and measured the cross-sectional area of the orbit, orbital fat, and each extra ocular muscle (EOM) except for the inferior oblique muscle 4 mm behind the eyeball. Each of the EOMs and orbital fat were calculated as a ratio to the total orbit area. A total of 0.1 cc of triamcinolone (40 mg/mL), dexamethasone (5 mg/mL), 5-FU, and BoNT-A (2.5 units) was injected transconjunctivally. Medical records were examined and photographs were utilized to assess MRD1, inferior palpebral fissure (IPF), and lid lag during down gaze before and after the injection. The patients were divided into two groups: responders (more than 1 mm decrease in MRD1 after injection) and non-responders. During the follow-up period (11.0 ± 11.6 months), any potential adverse effects were monitored. Results: CAS decreased from 3.0 ± 0.8 to 1.4 ± 0.5 after the injection, and MRD1 decreased from 5.0 ± 0.9 mm to 4.5 ± 1.3 mm. Sixty percent of the patients were responders. Before and after the injection, the difference between IPF and MRD1 in responders was 0.60 ± 1.10 mm and 0.90 ± 0.90 mm, respectively, whereas, in non-responders, it was −0.57 ± 0.88 mm and −0.15 ± 0.75 mm, respectively. In the responders, pre-injection IPF and FT4 were significantly higher (p < 0.05). Responders had a larger EOM cross-sectional area (153.5 ± 18.0 mm2), including a larger lateral rectus muscle cross-sectional area (37.6 ± 9.7 mm2) than non-responders (132.0 ± 27.9 mm2; 29.1 ± 8.1 mm2). In responders, the treatment effect on IPF and MRD1 remained consistent at 1.2 ± 3.4 mm and 1.2 ± 1.6 mm, respectively, during the latest follow-up assessment. Conclusions: The combination injection of corticosteroids, 5-FU, and BoNT-A would be effective, especially, in patients with hyperthyroidism and an elongated IPF. Additionally, an increase in EOM cross-sectional area on CT, up to 150 mm2, may serve as an additional positive indicator for the use of multimodal injections in UER with GO.

ASSESSMENT OF THYROID FUNCTION AND ULTRASONOGRAPHIC FINDINGS IN PATIENTS WITH MUCOPOLYSACCHARIDOSIS

Objective: The thyroid gland, with its high vascularity and low proliferation index of thyrocytes, is highly susceptible to storage diseases, however it has not been evaluated adequately in patients with in mucopolysaccharidosis (MPS). Therefore, the aim of this study is to assess the function, morphology, B- mode, and Doppler ultrasonography features of the thyroid gland in pediatric and adolescent patients with MPS and to evaluate whether the thyroid gland is involved in this disease. Material and Methods: Thyroid hormone functions were measured in all patients, and B-mode ultrasound and color Doppler imaging were performed. Results: Eight boys and 17 girls with MPS were included in the study. Eight patients were diagnosed with MPS I, 2 with MPS II, 3 with MPS III, 3 with MPS IVA, and 9 with MPS VI. Nineteen patients were receiving enzyme replacement therapy, while three patients diagnosed with MPS III remained untreated due to the unavailability of treatment options. Thyroid hormone levels were within normal limits for all patients. B-Mode ultrasound imaging revealed slightly heterogeneous echo texture in only 2 (8%) patients, both with MPS VI. Except for one patient with MPS VI, all color Doppler assessments were within normal limits. Conclusion: The results of our study demonstrate that both thyroid function tests and thyroid gland morphology are normal in MPS through childhood and adolescence. Therefore, we believe that thyroid gland dysfunction does not play a crucial role in the development of symptoms such as growth retardation, dry skin, coarse facial features, and intellectual disability, which could potentially be attributed to thyroid dysfunction. Instead, we think that these findings are more likely attributed to the primary disease involvement process

Trk-fused gene plays a critical role in diet-induced adipose tissue expansion and is also involved in thyroid hormone action.

Mutations in the Trk-fused gene (TFG) cause hereditary motor and sensory neuropathy with proximal dominant involvement, which reportedly has high co-incidences with diabetes and dyslipidemia, suggesting critical roles of the TFG in metabolism as well. We found that TFG expression levels in white adipose tissues (WATs) were elevated in both genetically and diet-induced obese mice and that TFG deletion in preadipocytes from the stromal vascular fraction (SVF) markedly inhibited adipogenesis. To investigate its role in vivo, we generated tamoxifen-inducible adipocyte-specific TFG knockout (AiTFG KO) mice. While a marked down-regulation of the peroxisome proliferator-activated receptor gamma target, de novo lipogenesis (DNL), and mitochondria-related gene expressions were observed in subcutaneous WAT (scWAT) from AiTFG KO mice, these effects were blunted in SVF-derived adipocytes when the TFG was deleted after differentiation into adipocytes, implying cell nonautonomous effects. Intriguingly, expressions of thyroid hormone receptors, as well as carbohydrate responsive element-binding protein β, which mediates the metabolic actions of thyroid hormone, were drastically down-regulated in scWAT from AiTFG KO mice. Reduced DNL and thermogenic gene expressions in AiTFG KO mice might be attributable to impaired thyroid hormone action in vivo. Finally, when adipocyte TFG was deleted in either the early or the late phase of high-fat diet feeding, the former brought about an impaired expansion of epididymal WAT, whereas the latter caused prominent adipocyte cell death. TFG deletion in adipocytes markedly exacerbated hepatic steatosis in both experimental settings. Collectively, these observations indicate that the TFG plays essential roles in maintaining normal adipocyte functions, including an enlargement of adipose tissue, thyroid hormone function, and thermogenic gene expressions, and in preserving hypertrophic adipocytes.

Measurement of salivary thyroid hormones using the LC-MS/MS technique in a clinical setting.

Saliva could be an attractive alternative to blood for assessing thyroid hormonal function. Our goal was to determine if the levels of thyroid hormones in saliva can accurately reflect a person's thyroid status and if they consistently correlate with the levels of the same hormones in the blood. We conducted a cross-sectional study. We enrolled a total of 109 participants with different thyroid conditions. We measured TSH (Thyroid-Stimulating Hormone), free T3 (fT3), and free T4 (fT4) in the blood using two different immunoassay methods: electrochemiluminescence immunoassay (ECLIA) and chemiluminescence immunoassay (CLIA). Saliva samples were collected using Salivette® tubes, and then we analyzed the levels of thyroid hormones in the saliva using liquid chromatography with tandem mass spectrometry (LC-MS/MS). Comparing salivary and serum levels of thyroid hormones, we observed significantly lower fT4 and higher fT3 levels in saliva (p < 0.001), regardless of the measurement method. We also found that salivary fT3 and fT4 levels were positively correlated in the entire group of participants (p < 0.001, R 0.575), as well as in those with TSH values within the normal reference range (p < 0.001, R 0.570). We further divided participants based on their TSH reference intervals and assessed the correlations between serum and salivary thyroid hormones within these groups. We also discovered that taking exogenous levothyroxine influenced the correlations between serum and salivary thyroid hormones. Thyroid antibodies did not have a significant impact on the levels of thyroid hormones in both serum and saliva. This study demonstrates that salivary thyroid hormones can partially reflect the levels of these hormones in the blood. Saliva may be a useful tool in a clinical setting for patients with thyroid antibodies, but it may not be as effective for those who are taking levothyroxine as a treatment.

In silico bioavailability triggers applied to direct and indirect thyroid hormone disruptors

Among endocrine disruption, interference with the thyroid hormone (TH) regulation is of increasing concern. Respective compounds encode through their structural features both the potential for TH disruption, and the bioavailability mitigating the toxicological effect. The aim of this study is to provide a substructure-based screening-level QSAR (quantitative structure-activity relationship) that discriminates bioavailable TH disruptors from not bioavailable counterparts, covering both direct and indirect (retinoid- and AhR-mediated) modes of action. The QSAR has been derived from literature data for 1642 compounds, and takes into account Lipinski's rule-of-five and the brain/blood partition coefficient Kbrain/blood. For its validation, an external test set of 145 substances has been used. For 1787 compounds meeting the model application domain, the model yields only one false negative. The discussion addresses the mechanistic meaning of the bioavailability triggers molecular weight, H-bond donor and acceptor, hydrophobicity (log Kow), and the physicochemical properties underlying log Kbrain/blood. The model may serve as bioavailability-screening step within a decision support system for the predictive assessment of chemicals regarding their potential to disrupt thyroid hormone function in a direct or indirect manner.

Effects of perchlorate and exogenous T4 exposures on body condition and endochondral ossification of Rana chensinensis tadpoles

Perchlorate, as an endocrine-disrupting chemical (EDC), is largely produced and used in the military, fireworks, fertilizers, and other industries and widely exists in water. Although perchlorate is known to destroy the normal function of thyroid hormones (THs) in amphibians and interfere with their growth and development, the impact of TH levels caused by sodium perchlorate (NaClO4) on endochondral ossification and skeletal development is poorly investigated, and the underlying molecular mechanism has not been clarified. The present study aimed to explore the potential effects of NaClO4 and exogenous thyroxine (T4) on the skeletal development of Rana chensinensis tadpoles and elucidate the related molecular mechanisms. Our results showed that histological changes occurred to the femur and tibia-fibula of tadpoles raised in 250 μg/L NaClO4 and 5 μg/L exogenous T4, and the length of their hindlimbs was significantly reduced. In addition, exogenous T4 exposure significantly interfered with the expression of Dio3, TRβ, MMP9, MMP13, and Runx2, inhibiting the endochondral ossification process. Therefore, we provide robust evidence that the changes in TH levels caused by NaClO4 and exogenous T4 will adversely affect the endochondral ossification and skeletal development of R. chensinensis tadpoles.

Congenital hypothyroidism in Bogotá, Colombia: acurrent description (2015-2021).

Congenital hypothyroidism (CH) is a decrease in thyroid hormone function in newborns, being one of theleading causes of neurological deficits and long-term metabolic complications. This study aims to determine the prevalence and characteristics of CH cases in Bogotá, Colombia, between 2015 and 2021, as notified through the mandatory report to the Public Health Surveillance System (PHSS). A retrospective cross-sectional study was conducted. All live births (LB) with a weight≥500 g, diagnosed with CH with or without goiter (ICD-10 codes E030 and E031, respectively) in Bogotá during 2015-2021 were analyzed. For a total of 201 cases, the prevalence rate was 3.29cases per 10,000 LB. 92.54 % were classified as isolated cases of CH, 4.48 % syndromic, and 2.98 % polymalformated. A total of 16.92 % was small for gestational age. The mean gestational age was 37.38weeks (SD 2.76), 26.87 % were preterm births. Among the mothers, 8.96 % suffered from pregnancy-related or chronic diseases, the most common being hypertensive disorders of pregnancy and pre-existant hypothyroidism (without clarity concerning etiology). Atotalof 66.67 % of cases did not receive treatment after diagnosis. Treatment was established by an average age of27days after birth (SD 36.02) and 17days after case notification to the PHSS (SD 36.13). Observed prevalence is similar to the rate reported by health authorities in Colombia but inferior to reports from high-income countries, highlighting the importance of improvements in the Colombian LB's screening program. Time to diagnosis and treatment was observed to be prolonged, suggesting that new pathways are required for timely CH treatment.

Sesamin alleviated fluoride – induced thyroid endocrine disruption in zebrafish (Danio rerio)

Previous studies have indicated that fluoride could induce the damage of thyroid. However, the effects of sesamin on thyroid endocrine function in zebrafish exposed to fluoride have not been clarified. This study was designed to investigate the alleviating effects of sesamin on thyroid endocrine disruption in zebrafish induced by fluoride. The results showed that sesamin significantly improved growth performance in adults exposed to fluoride; decreased significantly the mortality rate, increased remarkably the hatching rate and body length, and alleviated the phenomenon of spinal curvature, yolk cyst and pericardial cyst to varying degrees in fluoride-exposed embryos and larvae. Sesamin alleviated remarkably the damage of thyroid tissues in fluoride-exposed adults. Moreover, sesamin obviously reduced oxidative stress and improved the imbalance of thyroid hormones in fluoride-exposed adults or larvae. In addition, sesamin reversed the expression of endocrine-related genes of thyroid in fluoride-exposed adults or larvae. This indicates that sesamin can affects the thyroid tissue structure, hormone levels, and the expression of endocrine-related genes of thyroid, thus alleviating the thyroid endocrine disorder induced by fluoride and improving the growth and development. This study also demonstrates that sesamin can be a promising novel treatment for thyroid endocrine disorder caused by fluoride.

Association Between Thyroid-Stimulating Hormone Level and Bell's Palsy.

To investigate whether dysregulated thyroid hormone function is associated with Bell's palsy. Cross-sectional. Electronic medical record database of Clalit Health Services (CHS). CHS is an Israeli payer-provider, integrated health care system, serving >4.5 million members (54% of the Israeli population). Older than 18 years with Bell's palsy, during 2002 to 2019. None. A total of 1,374 patients with Bell's palsy who had thyroid-stimulating hormone (TSH) blood levels measured up to 60 days before the palsy were matched (1:2) for age and sex with 2,748 controls who had TSH blood levels and no history of Bell's palsy. Retrospective review of the CHS database, from 2002 to 2019 yielded 11,268 patients with Bell's palsy, of which, 1,374 met the inclusion criteria. Mean age was 57.9 years, and 61.4% were female. A higher percentage of patients in the Bell's palsy group had low TSH (≤0.55 mIU/L) compared with controls (5.7% vs. 3.6%, p < 0.001). Low TSH compared with TSH > 0.55 mIU/L, was independently associated with 1.45-fold increased odds for having Bell's palsy (95% CI 1.11-2.02, p < 0.001), when controlled for age, sex, body mass index, diabetes, hypertension, prior cerebrovascular accident, hemoglobin level, and purchasing thyroid hormone drugs. Among the patients with TSH ≤ 0.55 mIU/L, 95.5% had normal free thyroxin and 97.7% had normal free triiodothyronine levels (subclinical hyperthyroidism). For 47.1% of patients, TSH remained ≤0.55 mIU/L, 3 to 12 months after the Bell's palsy occurred and most patients had normal free thyroxin (95.4%) and normal free triiodothyronine (91.8%). Subclinical hyperthyroidism is independently associated with Bell's palsy after controlling for multiple confounding factors.

Toxic or beneficial? What is the role of food‐relevant selenium species selenoneine?

Toxic or beneficial? What is the role of food‐relevant selenium species selenoneine?

Hemodialysis and thyroid disorders in chronic kidney disease patients at General Hospital of Douala, Cameroon

Background: kidneys' physiology is related to thyroid hormone functions. They play an important role in certain pathways of these hormones. Therefore the decline in renal function is accompanied by changes in thyroid function. Thyroid abnormalities are described in chronic hemodialysis but insufficiently elucidated in our area. Hence our interest was to evaluate thyroid function in chronic kidney disease patients to point out the implication of hemodialysis on thyroid dysfunction in our population. Method: we carried out a thyroid function test on a chronic hemodialysed patient admitted at Douala General Hospital (DGH) nephrology service for chronic kidney failure. Samples collected were tested for thyroid hormones total T3 (triiodothyronine), total T4 (thyroxine), and TSH (Thyroid Stimulating Hormone) using enzyme-linked immunosorbent assay (ELISA) technic. Epi Info was used for statistical analysis and 0.05 was significance threshold. Results: most of the participants were male-gendered (62.2%). The mean age was 49 years (41 ± 12.90) ranging from 20 and 79 years. Thyroid profile analysis of each patient highlighted 30 cases of hypothyroidism (36.59%) and 2 cases of hyperthyroidism (2.44%) out of the 82 enrolled subjects. Besides, our results showed that the duration of dialysis (P = 0.019) and old age (P = 0.04) were risk factors associated with hypothyroidism. Other factors such as gender and clinical history had no impact on the patient's thyroid status. Conclusion: our study indicated that hypothyroidism is a common endocrine disorder in patients who were going through chronic hemodialysis. A large population size study can be useful to set up systematic thyroid hormone checkups among chronic hemodialysis patients to improve population health conditions.

Prevalence and clinical correlates of abnormal lipid metabolism in first-episode and drug-naïve patients with major depressive disorder with abnormal glucose metabolism

Comorbid glucose metabolism abnormalities are very common in patients with major depressive disorder (MDD), and glucose metabolism and lipid metabolism are closely related. However, there are few researches on the incidence and related factors of lipid metabolism abnormalities among MDD patients with comorbid glucose metabolism abnormalities. A cross-sectional study involving 1718 first-episode and drug-naïve (FEDN) MDD patients was conducted. The 17-item Hamilton Depression Scale (HAMD-17), Hamilton Anxiety Rating Scale (HAMA) and Positive and Negative Syndrome Scale (PANSS) positive subscale were utilized to evaluate depressive, anxiety and psychotic symptom, respectively. Serum thyroid function-related parameters, glucose- and lipid-metabolism parameters were measured. The prevalence of abnormal lipid metabolism was significantly higher in FEDN MDD patients with abnormal glucose metabolism than in those without abnormal glucose metabolism (P < 0.001). In MDD patients with abnormal glucose metabolism, TSH, FT3 and body mass index (BMI) levels were significantly higher in the abnormal lipid metabolism subgroup than in the non-abnormal lipid metabolism subgroup. Binary logistic regression analysis showed that TSH, FT3 and BMI were the influencing factors of abnormal lipid metabolism in MDD patients with abnormal glucose metabolism (all P < 0.05). MDD patients with abnormal glucose metabolism have a high prevalence of abnormal lipid metabolism. Moreover, abnormal glucose metabolism was an independent risk factor for abnormal lipid metabolism in patients with MDD. In addition, thyroid hormone function and BMI may contribute to the co-occurrence of abnormal lipid metabolism in MDD patients with abnormal glucose metabolism.