A Selenium-Containing Catalytic Antibody with Type I Deiodinase Activity

2001 ◽  
Vol 283 (5) ◽  
pp. 1007-1012 ◽  
Author(s):  
Gewei Lian ◽  
Lan Ding ◽  
Mo Chen ◽  
Liyan Liu ◽  
Daqing Zhao ◽  
...  
2001 ◽  
Vol 285 (1) ◽  
pp. 159
Author(s):  
Gewei Lian ◽  
Lan Ding ◽  
Mo Chen ◽  
Liyan Liu ◽  
Daqing Zhao ◽  
...  

Endocrinology ◽  
1989 ◽  
Vol 124 (2) ◽  
pp. 740-745 ◽  
Author(s):  
SEBO JAN EELKMAN ROODA ◽  
ELLEN KAPTEIN ◽  
MARJA RUTGERS ◽  
THEO J. VISSER

1989 ◽  
Vol 259 (2) ◽  
pp. 555-559 ◽  
Author(s):  
M Giralt ◽  
L Casteilla ◽  
O Viñas ◽  
T Mampel ◽  
R Iglesias ◽  
...  

Iodothyronine 5'-deiodinase activity appears to be a type I enzyme in bovine brown adipose tissue, on the basis of its high Km for 3,3',5'-tri-iodothyronine (‘reverse T3’) (in the micromolar range) and sensitivity to propylthiouracil inhibition. This enzyme activity is already detectable in perirenal adipose tissue of bovine fetuses in the second month of gestation, reaches peak values around the seventh month of fetal life, declines before birth, becomes lower after parturition and finally undetectable in the adult cow. Iodothyronine 5'-deiodinase activity is present in the pericardic, peritoneal and intermuscular adipose depots of the neonatal calf, but it is always undetectable in the subcutaneous adipose tissue. It is concluded that iodothyronine 5'-deiodinase is a specific feature of brown fat in the bovine species that is not shared by white adipose tissue. white adipose tissue. Peak values of 5'-deiodinating activity appear as an early event in the prenatal differentiation programme of bovine brown-fat cells as they occur when uncoupling-protein-gene expression first starts.


2003 ◽  
Vol 284 (6) ◽  
pp. E1172-E1176 ◽  
Author(s):  
Patricia Cristina Lisboa ◽  
Karen Jesus Oliveira ◽  
Adriana Cabanelas ◽  
Tania Maria Ortiga-Carvalho ◽  
Carmen Cabanelas Pazos-Moura

We investigated the effect of acute cold exposure, leptin, and the somatostatin analog octreotide (OCT) on thyroid type I (D1) and II (D2) deiodinase activities. Microsomal D1 and D2 activities were measured by the release of 125I from 125I-reverse triiodothyronine (rT3) under different assay conditions. Rats exposed to 4°C (15, 30, 60, and 120 min) showed progressive reduction in thyroidal D1 and D2, reaching ∼40% at 2 h ( P < 0.05) despite increased circulating TSH ( P < 0,05) associated with the higher thyroid D1 and D2 in hypothyroid rats. A single injection of leptin (8 μg/100 g body wt sc) induced increased thyroid and liver D1 ( P < 0.05), but not thyroid D2, activities at 30 and 120 min, independently of the serum TSH rise shown only at 2 h. OCT (1 μg/kg body wt sc) increased D1 and D2 activity significantly 24 h after a single injection, with no changes in serum TSH. Therefore, leptin and somatostatin are potential physiological upregulators of thyroid deiodinases, and their low secretion during acute cold exposure may be a potential mechanism contributing to cold-induced reduction in thyroid deiodinase activity.


2004 ◽  
Vol 1018 (1) ◽  
pp. 219-223 ◽  
Author(s):  
JÚLIUS BRTKO ◽  
DANA MACEJOVÁ ◽  
JÁN KNOPP ◽  
RICHARD KVETŇANSKÝ
Keyword(s):  
Type I ◽  

1992 ◽  
Vol 133 (1) ◽  
pp. 45-49 ◽  
Author(s):  
P. H. L. M. Geelhoed-Duijvestijn ◽  
F. Roelfsema ◽  
J. P. Schröder-van der Elst ◽  
J. van Doorn ◽  
D. van der Heide

ABSTRACT We have studied the effects of the administration of GH on plasma levels and peripheral production of tri-iodothyronine (T3) from thyroxine (T4) in thyroidectomized male Wistar rats given a continuous i.v. infusion of T4 (1 μg/100 g body weight per day) and GH (120 μg per day) for 3 weeks. Tracer doses of 131I-labelled T3 and 125I-labelled T4 were added to the infusion. At isotopic equilibrium (10 days after the addition of 125I-labelled T4) the rats were bled and perfused. The plasma appearance rate for T3 was higher (10·6±1·3 vs 8·4 ± 2·8 pmol/h per 100 g body weight, P = 0·05) and plasma TSH was lower (246±24 vs 470±135 pmol/l, P<0·01) in GH-treated rats. The amount of T3 in liver (12·3 ±2·8 vs 5·5 ± 1·7 pmol/g wet weight, P<0·01), kidney (11·5±1·4 vs 6·5± 1·4 pmol/g wet weight, P <0·01) and pituitary (8·8 ±2·7 vs 4·8±0·5 pmol/g wet weight, P< 0·01) was higher than in controls, mainly as a result of an increased local production of T3 from T4, but plasma-derived T3 was also higher in most organs. We found an increased intracellular T3 concentration in the pituitary which may be responsible for the lower plasma TSH concentration in the GH-treated rats. Since the increase in locally produced T3 is found particularly in liver, kidney and pituitary, typical organs that express 5′-deiodinase activity, we suggest that GH acts on thyroid hormone metabolism by stimulating type-I deiodinase activity. Journal of Endocrinology (1992) 133, 45–49


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