Molecular Insights into the Possible Role of Kir4.1 and Kir5.1 in Thyroid Hormone Biosynthesis

2015 ◽  
Vol 83 (2) ◽  
pp. 141-147 ◽  
Author(s):  
Helton Estrela Ramos ◽  
Magnus R�gios Dias da Silva ◽  
Aurore Carr� ◽  
Joaquim Cust�dio Silva Jr. ◽  
Rolf Matias Paninka ◽  
...  
1978 ◽  
Vol 88 (1) ◽  
pp. 87-93 ◽  
Author(s):  
Anne du Breuil ◽  
Valerie Anne Galton

ABSTRACT The importance of the monodeiodination of T4 to T3 in the physiological action of T4 was explored by assessing the role of T4 in maintaining propylthiouracil (PTU)-treated rats during exposure to 4°C. (PTU inhibits both thyroid hormone biosynthesis and T4 to T3 conversion in peripheral tissues.) Firstly, the effects of cold exposure on the metabolism of T4 in control and PTU-treated rats equilibrated with [125I]T4 (2 μg/100 g b. w./day) were determined. PTU was administered in the food (2 mg/g food). In control rats, no significant changes in T4 metabolism occurred during 3 days at 4°C. Urinary 125I was greatly decreased in PTU-treated rats. Exposure of these rats to cold resulted in some increase but values were still 50 % below normal. Secondly, four groups of rats were exposed to cold: control; PTU-treated; T4-treated; PTU + T4-treated. Control and T4-treated rats survived. PTU-treated rats died unless T4 was administered. Radioimmunoassay of T4 and T3 indicated significant concentrations of T3 in sera of rats from all but the PTU + T4 group. These results suggest that T4 permits survival in the cold-exposed PTU-treated rat without being converted to T3 and thus they support the concept that T4 has intrinsic biological activity.


Endocrinology ◽  
1968 ◽  
Vol 83 (6) ◽  
pp. 1253-1258 ◽  
Author(s):  
LESLIE J. DEGROOT ◽  
STEPHANIE JAKSINA ◽  
MADHU KARMARKAR

2009 ◽  
Vol 130 (1) ◽  
pp. 72-85 ◽  
Author(s):  
K. Wang ◽  
Y. N. Sun ◽  
J. Y. Liu ◽  
L. Zhang ◽  
Y. Ye ◽  
...  

Author(s):  
Azhari Gani ◽  
Iskandar Zakaria

Congenital hypothyroid (CH) is a Hormonal disorder that can be caused by thyroid gland dysfunction and if not treated early on, will cause serious mental and physical growth disorders. CH is divided into permanent and transient forms which etiologically can be divided into primary, secondary or peripheral. Thyroid dysgenesis is the primary cause and 85% of permanent CH is with abnormalities of thyroid hormone biosynthesis from birth (dishormongeneses). The incidence of dysgenesis accounts for 10-15% of cases. Transient congenital thyroid occurs mostly in infants with preterm birth in low-iodine endemic areas. A study showed a permanent incidence of CH 1: 1500 and transient CH 1: 300 in one of the areas with iodine deficiency in Central Java.Survival analysis showed that the risk of developing mental retardation and delayed physical growth was greater at the age of diagnosis over 1 year.


2019 ◽  
Vol 2019 (4) ◽  
Author(s):  
Albert Van der Vliet

The two DUOX enzymes were originally identified as participating in the production of hydrogen peroxide as a pre-requisite for thyroid hormone biosynthesis in the thyroid gland [6].NOX enzymes function to catalyse the reduction of molecular oxygen to superoxide and various other reactive oxygen species (ROS). They are subunits of the NADPH oxidase complex.


Author(s):  
Mary Lee Gregory

Congenital hypothyroidism (CH) results from the effects of insufficient thyroid hormone on the developing fetus and infant, and is characterized by severe intellectual disability and growth inhibition. CH can result from maternal iodine deficiency, which can be abolished by appropriate dietary iodine supplementation. Alternately, CH may be caused by congenital defects of the thyroid gland and thyroid hormone biosynthesis abnormalities (primary congenital hypothyroidism), or by “central hypothyroidism,” in which the brain produces insufficient thyroid stimulating hormone. Treatment of these latter etiologies requires administration of thyroid hormone.


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