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has not been fully established, and may be defined as a thyroid-stimulating hormone (TSH) level above the upper limit of the reference range, under a daily LT4 dose of ≥1.9 µg/kg ( 4 ). Actually, some patients still exhibit refractory hypothyroidism
Intensive Care Unit, Hospital de Clínicas de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil
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Internal Medicine Division, Hospital de Clínicas de Porto Alegre, Internal Medicine Department, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil
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(T4), and elevated plasma levels of the inactive hormone reverse T3 (rT3) in the presence of normal thyrotropin (TSH) levels ( 1 ). The pathophysiology of NTIS is multifactorial. In the early phase, the peripheral TH metabolism is impaired, with
Department of Endocrinology and Metabolism, People's Hospital of Liaoning Province, Shenyang, People’s Republic of China
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Department of Laboratory Medical, The First Hospital of China Medical University, Shenyang, People’s Republic of China
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Introduction Subclinical hypothyroidism (SCH), characterized by elevated levels of thyroid-stimulating hormone (TSH) with total thyroxine (TT4) within the normal reference range, is the most common type of thyroid disorder in pregnancy ( 1
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adulthood ( 2 , 5 , 6 ). Thyroid hormones can regulate metabolism associated with basal metabolic rate and body composition ( 7 , 8 ). In general, the thyroid-stimulating hormone (TSH) is positively correlated with BMI, whereas total thyroxine (TT4) and
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vacutainers at the initial visit. Each blood sample was analysed for TSH, free tri-iodothyronine (FT 3 ), free T 4 (FT 4 ) and anti-TPO by electro-chemiluminescence immunoassay (ELECSYS-2010, Roche–Hitachi Diagnostics). The reference range for the above
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Introduction Subclinical hypothyroidism (SH) is a biochemical condition defined as serum thyroid-stimulating hormone (TSH) exceeding the limit of its reference range by age, while the concentration of serum free thyroxin (FT4) remains within
Department of Psychology II, University of Lübeck, Lübeck, Germany
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Department of Endocrinology, The Christie, University of Manchester, Manchester, UK
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Department of Psychology II, University of Lübeck, Lübeck, Germany
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determination of TSH, which is generally normal, or slightly elevated in some cases. However, free thyroxine (fT4) is universally elevated ( 4 ). In RTHβ, the sensitivity of the hypothalamic–pituitary axis to thyroid hormone is reduced, due to altered signalling
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Background: Signal transducer and activator of transcription 6 (STAT6) is an important nuclear transcription factor. Previous study demonstrated that blockading STAT6 can ameliorate thyroid function by reducing serum T3 and T4. Sodium/iodide symporter (NIS) is a key protein that mediates active iodine uptake and plays an important role in regulating thyroid function. This study explored the interaction between STAT6 and NIS.
Methods: Immunohistochemical staining was performed for detecting the expression of NIS in different tissues. Reverse transcription-polymerase chain reaction (RT-PCR) was performed for evaluating the mRNA level of NIS when Nthy-ori 3-1cells were incubated with IL4, TSH (Thyroid stimulating hormone) or monoclonal TSAb (thyroid-specific stimulatory autoantibody) for 24h. Quantitative RT-PCR,Western blot and immunofluorescence analysis were performed for detecting NIS expression after inhibiting STAT6 phosphorylation by AS1517499. Finally, we used Luciferase reporter assays to explore the ability of STAT6 to regulate the promoter activity of the NIS-coding gene.
Results: NIS was highly expressed in thyroid epithelial cells of EAGD mice or Graves' disease (GD) patients and TSAb increased the expression of NIS. We show that STAT6 phosphorylation inhibitor can attenuate the effect of TSAb on increasing NIS protein and mRNA levels. Finally, we confirm that transcription factor STAT6 can mediate NIS transcription and co-activator P100 protein can enhance STAT6-dependent transcriptional activation.
Conclusion: In Graves' disease, TSAb induces STAT6 signaling to upregulate NIS expression and STAT6 blockade ameliorates thyroid function via downregulation of the sodium/iodide symporter. Our study furthers understanding of the effects of STAT6 on thyroid function and reveals new avenues for GD treatment.
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Department of Endocrinology, Diabetes and Metabolism, Centro Hospitalar S. João, Alameda Professor Hernâni Monteiro, Porto, Portugal
Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal
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Department of Endocrinology, Diabetes and Metabolism, Centro Hospitalar S. João, Alameda Professor Hernâni Monteiro, Porto, Portugal
Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal
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Introduction Subclinical hypothyroidism (SCH) is diagnosed biochemically when both serum-free thyroxine (FT4) and free triiodothyronine (FT3) are within the normal range, whereas the serum thyroid-stimulating hormone (TSH) is elevated ( 1
Department of Clinical Biochemistry, Aalborg University Hospital, Aalborg, Denmark
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Department of Clinical Biochemistry, Aalborg University Hospital, Aalborg, Denmark
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Department of Geriatrics, Aalborg University Hospital, Aalborg, Denmark
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Department of Clinical Biochemistry, Aalborg University Hospital, Aalborg, Denmark
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hypothyroidism seen as part of Hashimoto’s thyroiditis (HT) ( 2 ). In GD, antibodies against the thyroid-stimulating hormone (TSH) receptor (TRAb) stimulate the thyroid gland to an increased production of thyroid hormone that causes the biochemical