scholarly journals Functions of the Thyroid-Stimulating Hormone on Key Developmental Features Revealed in a Series of Zebrafish Dyshormonogenesis Models

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1984
Author(s):  
Jia Song ◽  
Yao Lu ◽  
Xiaoxia Cheng ◽  
Chuang Shi ◽  
Qiyong Lou ◽  
...  
Keyword(s):  
Growth Retardation ◽  
Gonad Development ◽  
Thyroid Stimulating Hormone ◽  
Sex Characteristics ◽  
Developmental Defects ◽  
Secondary Sex Characteristics ◽  
Fin Ray ◽  
Hpt Axis ◽  
Developmental Features ◽  
Stimulating Hormone

The hypothalamic–pituitary–thyroid (HPT) axis regulates many critical features in vertebrates. Utilizing TALENs and CRISPR/Cas9 techniques, thyroid-stimulating hormone subunit beta a (tshba), thyroglobulin (tg), and solute carrier family 16 member 2 (slc16a2) mutant zebrafish lines were generated. Among the three mutants, the earliest time point for the significantly altered T3 contents was observed in tshba mutants, which resulted in the most severe defects, including typical defects such as the retardation of inflated anterior swimming bladder (aSB), proper formation of fin ray and posterior squamation (SP), the larval-to-juvenile transition (LTJT) process, juvenile growth retardation, and mating failure. In tg mutants, which are actually compensated with an alternative splicing form, growth retardation was observed in the juvenile stage without LTJT and reproductive defects. The evident goiter phenotype was only observed in tg- and slc16a2 mutants, but not in tshba mutants. Other than goiters being observed, no other significant developmental defects were found in the slc16a2 mutants. Regarding the reproductive defects observed in tshba mutants, the defective formation of the secondary sex characteristics (SSCs) was observed, while no obvious alterations during gonad development were found. Based on our analyses, zebrafish at the 6–12 mm standard length or 16–35 days post-fertilization (dpf) should be considered to be in their LTJT phase. Using a series of zebrafish dyshormonogenesis models, this study demonstrated that the TSH function is critical for the proper promotion of zebrafish LTJT and SSC formation. In addition, the elevation of TSH levels appears to be essential for goiter appearance in zebrafish.

scholarly journals Low free thyroxine and normal thyroid-stimulating hormone in infants and children: possible causes and diagnostic work-up

2021 ◽  
Author(s):  
Peter Lauffer ◽  
A. S. Paul van Trotsenburg ◽  
Nitash Zwaveling-Soonawala
Keyword(s):  
Thyroid Hormone ◽  
Hormone Receptor ◽  
Thyroid Hormone Receptor ◽  
Thyroid Stimulating Hormone ◽  
Free Thyroxine ◽  
Infants And Children ◽  
Clinical Algorithm ◽  
Hpt Axis ◽  
In Infants And Children ◽  
Stimulating Hormone

AbstractScreening for hypo- or hyperthyroidism in adults is generally done by measuring the serum thyrotropin (thyroid-stimulating hormone, TSH) concentration. This is an efficient approach in case of suspected acquired thyroid disease. However, in infants and children, congenital hypothalamus-pituitary-thyroid (HPT) axis disorders also need to be considered, including primary and central congenital hypothyroidism, and even rarer thyroid hormone receptor and transporter defects. In primary congenital hypothyroidism, TSH will be elevated, but in the other congenital HPT axis disorders, TSH is usually within the normal range. Free thyroxine (FT4) assessment is essential for the diagnosis in these conditions.Conclusion: Here we discuss a number of rare congenital HPT axis disorders in which TSH is normal, but FT4 is low, and provide a clinical algorithm to distinguish between these disorders. What is Known:• A single thyroid-stimulating hormone (TSH) measurement is an appropriate screening method for primary hypothyroidism.• For central hypothyroidism and rare thyroid hormone receptor and transporter defects a free thyroxine (FT4) measurement is essential for the diagnosis because TSH is usually normal. What is New:• Here we present a new problem-oriented clinical algorithm including a diagnostic flow-chart for low FT4 and normal TSH in infants and children.

scholarly journals An Update on the Pathophysiology and Diagnosis of Inappropriate Secretion of Thyroid-Stimulating Hormone

2021 ◽  
Vol 22 (12) ◽  
pp. 6611
Author(s):  
Kenji Ohba
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormone Receptor ◽  
Elevated Serum ◽  
Thyroid Stimulating Hormone ◽  
Free Triiodothyronine ◽  
Related Condition ◽  
Important Indicator ◽  
Inappropriate Secretion ◽  
Hpt Axis ◽  
Stimulating Hormone

Inappropriate secretion of thyroid-stimulating hormone (IST), also known as central hyperthyroidism, is a clinical condition characterized by elevated free thyroxine and triiodothyronine concentrations concurrent with detectable thyroid-stimulating hormone (TSH) concentrations. Similarly, the term syndrome of IST (SITSH) is widely used in Japan to refer to a closely related condition; however, unlike that for IST, an elevated serum free triiodothyronine concentration is not a requisite criterion for SITSH diagnosis. IST or SITSH is an important indicator of resistance to thyroid hormone β (RTHβ) caused by germline mutations in genes encoding thyroid hormone receptor β (TRβ) and TSH-secreting pituitary adenoma. Recent evidence has accumulated for several conditions associated with IST, including RTH without mutations in the TRβ gene (non-TR-RTH), the phenomenon of hysteresis involving the hypothalamus-pituitary-thyroid axis (HPT-axis), methodological interference, and Cushing’s syndrome after surgical resection. However, little information is available on the systematic pathophysiological aspects of IST in previous review articles. This report presents an overview of the recent advances in our understanding of the etiological aspects of IST that are relevant for diagnosis and treatment. Moreover, the report focuses on the potential mechanism of IST caused by hysteresis in the HPT-axis (lagging TSH recovery) in terms of epigenetic regulation.

Familial Growth Retardation with Isolated Thyroid-Stimulating Hormone Deficiency

1984 ◽  
Vol 23 (12) ◽  
pp. 675-678 ◽  
Author(s):  
A. Labbe ◽  
C. Dubray ◽  
G. Gaillard ◽  
G. Besse ◽  
P. Assali ◽  
...  
Keyword(s):  
Growth Retardation ◽  
Thyroid Stimulating Hormone ◽  
Hormone Deficiency ◽  
Stimulating Hormone

CLINICAL EVALUATION OF THE THYROID STIMULATING HORMONE ACTIVITY IN EXOPHTHALMOS

1961 ◽  
Vol 38 (4) ◽  
pp. 577-584 ◽  
Author(s):  
Sven Erik Björkman ◽  
Torsten Denneberg ◽  
Inge Hedenskog
Keyword(s):  
Clinical Evaluation ◽  
Thyroid Stimulating Hormone ◽  
Significant Rise ◽  
Hormone Activity ◽  
Control Subjects ◽  
Long Duration ◽  
Stimulating Factor ◽  
Stimulating Hormone

ABSTRACT A method for demonstrating the presence of a thyroid stimulating factor in the blood of patients with progressive exophthalmos after thyroidectomy or after treatment with radioiodine is described. The method consists of transfusing freshly drawn blood from the patients to euthyroid recipients and subsequently following the PBI level of the recipients at regular intervals. Six exophthalmic patients tested in this manner were found to have such a factor in their circulating blood. After transfusion of their blood a significant rise in the PBI level of the recipients could be demonstrated. Two other patients, one with exophthalmos of long duration did not show this response nor did it occur after transfusion of blood from two control subjects. In one case the action of this factor was compared with that of animal thyrotrophin and found to be of the same magnitude.

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