Thyroid hormone analog inhibition of hepatic 5′-iodothyrohine deiodinase activity

1988 ◽  
Vol 11 (9) ◽  
pp. 657-661 ◽  
Author(s):  
B. L. Shulkin ◽  
M. B. Bolger ◽  
R. D. Utiger
Keyword(s):  
Thyroid Hormone ◽  
Deiodinase Activity ◽  
Hormone Analog

Pilot Studies on the Use of 3,5-Diiodothyropropionic Acid, a Thyroid Hormone Analog, in the Treatment of Congestive Heart Failure

Cardiology ◽  
2002 ◽  
Vol 97 (4) ◽  
pp. 218-225 ◽  
Author(s):  
Eugene Morkin ◽  
Gregory Pennock ◽  
Peter H. Spooner ◽  
Joseph J. Bahl ◽  
Katherine Underhill Fox ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Thyroid Hormone ◽  
Pilot Studies ◽  
Hormone Analog

scholarly journals Placental 5-Deiodinase Activity and Fetal Thyroid Hormone Economy Are Unaffected by Selenium Deficiency in the Rat

1993 ◽  
Vol 34 (3) ◽  
pp. 288-292 ◽  
Author(s):  
Jean-Pierre Chanoine ◽  
Sharon Alex ◽  
Scott Stone ◽  
Shih Lieh Fang ◽  
Irini Veronikis ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Selenium Deficiency ◽  
Deiodinase Activity ◽  
Fetal Thyroid

DITPA, A Thyroid Hormone Analog, Reduces Infarct Size and Attenuates the Inflammatory Response Following Myocardial Ischemia

2011 ◽  
Vol 171 (2) ◽  
pp. 379-385 ◽  
Author(s):  
Abdelrahman A. Abohashem-Aly ◽  
Xianzhong Meng ◽  
Jilin Li ◽  
Miral R. Sadaria ◽  
Lihua Ao ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Myocardial Ischemia ◽  
Inflammatory Response ◽  
Infarct Size ◽  
Hormone Analog

scholarly journals Effect of excessive iodine exposure on the placental deiodinase activities and Hoxc8 expression during mouse embryogenesis

2007 ◽  
Vol 98 (1) ◽  
pp. 116-122 ◽  
Author(s):  
Xue F. Yang ◽  
Jian Xu ◽  
Huai L. Guo ◽  
Xiao H. Hou ◽  
Li P. Hao ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormone Receptor ◽  
Skeletal Development ◽  
Gene Expression Pattern ◽  
Skeletal Malformation ◽  
Thyroid Hormone Metabolism ◽  
Deiodinase Activity ◽  
Excessive Iodine ◽  
Total Thyroxine

Excessive iodine induces thyroid dysfunction. However, the effect of excessive iodine exposure on maternal–fetal thyroid hormone metabolism and on the expression of genes involved in differentiation, growth and development is poorly understood. Since a thyroid hormone receptor response element was found in the Hoxc8 promoter region, Hoxc8 expression possibly regulated by excessive iodine exposure was firstly investigated. In the present study, Balb/C mice were given different doses of iodine in the form of potassium iodate (KIO3) at the levels of 0 (sterile water), 1·5, 3·0, 6·0, 12·0 and 24·0 μg/ml in drinking water for 4 months, then were mated. On 12·5 d postcoitum, placental type 2 and type 3 deiodinase activities and fetal Hoxc8 expression were determined. The results showed that excessive iodine exposure above 1·5 μg/ml resulted in an increase of total thyroxine and a decrease of total triiodothyronine in the serum of maternal mice, which was mainly associated with the inhibition of type 1 deiodinase activity in liver and kidney. Placental type 2 deiodinase activity decreased, showing an inverse relationship with maternal thyroxine level. Hoxc8 mRNA and protein expression at 12·5 d postcoitum embryos were down regulated. Because Hoxc8 plays an important role in normal skeletal development, this finding provides a possible explanation for the skeletal malformation induced by excessive iodine exposure and also provides a new clue to study the relationship between iodine or thyroid hormones and Hox gene expression pattern.

The thyroid hormone analog DITPA restoresI to in rats after myocardial infarction

2000 ◽  
Vol 278 (4) ◽  
pp. H1105-H1116 ◽  
Author(s):  
Alan D. Wickenden ◽  
Roger Kaprielian ◽  
Xiao-Mang You ◽  
Peter H. Backx
Keyword(s):  
Myocardial Infarction ◽  
Thyroid Hormone ◽  
Action Potential ◽  
Ventricular Myocytes ◽  
Monophasic Action Potential ◽  
Mrna Levels ◽  
Hormone Analog ◽  
Life Threatening ◽  
The Right

Previous studies have established that reductions in repolarizing currents occur in heart disease and can contribute to life-threatening arrhythmias in myocardium. In this study, we investigated whether the thyroid hormone analog 3,5-diiodothyropropionic acid (DITPA) could restore repolarizing transient outward K+ current ( I to) density and gene expression in rat myocardium after myocardial infarction (MI). Our findings show that I to density was reduced after MI (14.0 ± 1.0 vs. 10.2 ± 0.9 pA/pF, sham vs. post-MI at +40 mV). mRNA levels of Kv4.2 and Kv4.3genes were decreased but Kv1.4 mRNA levels were increased post-MI. Corresponding changes in Kv4.2 and Kv1.4 protein were also observed. Chronic treatment of post-MI rats with 10 mg/kg DITPA restored I to density (to 15.2 ± 1.1 pA/pF at +40 mV) as well as Kv4.2 and Kv1.4 expression to levels observed in sham-operated controls. Other membrane currents (Na+, L-type Ca2+, sustained, and inward rectifier K+ currents) were unaffected by DITPA treatment. Associated with the changes in I toexpression, action potential durations (current-clamp recordings in isolated single right ventricular myocytes and monophasic action potential recordings from the right free wall in situ) were prolonged after MI and restored with DITPA treatment. Our results demonstrate that DITPA restores I to density in the setting of MI, which may be useful in preventing complications associated with I to downregulation.

Inhibition of Type 1 Iodothyronine Deiodinase by Bisphenol A

2019 ◽  
Vol 51 (10) ◽  
pp. 671-677 ◽  
Author(s):  
Maurício Martins da Silva ◽  
Carlos Frederico Lima Gonçalves ◽  
Leandro Miranda-Alves ◽  
Rodrigo Soares Fortunato ◽  
Denise P. Carvalho ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Thyroid Hormone ◽  
Bisphenol A ◽  
Brown Adipose Tissue ◽  
Tissue Type ◽  
Deiodinase Activity ◽  
Brown Adipose

AbstractPlastics are ubiquitously present in our daily life and some components of plastics are endocrine-disrupting chemicals, such as bisphenol A and phthalates. Herein, we aimed to evaluate the effect of plastic endocrine disruptors on type 1 and type 2 deiodinase activities, enzymes responsible for the conversion of the pro-hormone T4 into the biologically active thyroid hormone T3, both in vitro and in vivo. Initially, we incubated rat liver type 1 deiodinase and brown adipose tissue type 2 deiodinase samples with 0.5 mM of the plasticizers, and the deiodinase activity was measured. Among them, only BPA was capable to inhibit both type 1 and type 2 deiodinases. Then, adult male Wistar rats were treated orally with bisphenol A (40 mg/kg b.w.) for 15 days and hepatic type 1 deiodinase and brown adipose tissue type 2 deiodinase activities and serum thyroid hormone concentrations were measured. In vivo bisphenol A treatment significantly reduced hepatic type 1 deiodinase activity but did not affect brown adipose tissue type 2 deiodinase activity. Serum T4 levels were higher in bisphenol A group, while T3 remained unchanged. T3/T4 ratio was decreased in rats treated with bisphenol A, reinforcing the idea that peripheral metabolism of thyroid hormone was affected by bisphenol A exposure. Therefore, our results suggest that bisphenol A can affect the metabolism of thyroid hormone thus disrupting thyroid signaling.

Diminished hepatic triiodothyronine production in Gunn rats

1986 ◽  
Vol 113 (2) ◽  
pp. 281-288 ◽  
Author(s):  
J. R. Saltzman ◽  
D. W. Clark ◽  
R. D. Utiger
Keyword(s):  
Thyroid Hormone ◽  
Rat Liver ◽  
Liver Homogenate ◽  
Unconjugated Bilirubin ◽  
Thyroid Hormone Metabolism ◽  
Gunn Rats ◽  
Deiodinase Activity ◽  
Sediment Fraction ◽  
Liver Homogenates

Abstract. The liver is a major site of conversion of thyroxine (T4) to the more active thyroid hormone 3,5,3'-triiodothyronine (T3). Hepatic T4 to T3 conversion is altered by a variety of pathological processes and pharmacological agents. We studied T4 to T3 conversion in glucuronyl transferase deficient homozygous Gunn rats because they have a hepatic enzyme abnormality which leads to hyperbilirubinaemia, and also because they have been reported to have alterations in thyroid hormone metabolism. An in vitro incubation system employing the 10 000 × g supernatant of liver homogenate was used, and T3 production was measured by radioimmunoassay. Experiments were done using substrate concentrations ranging from 0.56 to 20 μm, tissue protein in concentrations ranging from 0.625 to 20 mg and incubation times of 15 to 60 min. T3 production by liver homogenates from homozygous Gunn rats in these studies ranged from 29 to 70% of that produced by liver homogenates from phenotypically normal heterozygous Gunn rats. The deficit in hepatic T3 production by homozygous rats could not be overcome by increasing cofactor concentrations. After ultracentrifugation at 100 000 μ g, T4-5'-deiodinase activity was found primarily in the 100 000 × g sediment fraction. Homogygous rat liver 100 000 × g sediment T3 production was 55% of that of the heterozygous rat liver 100 000 × g sediment. Liver cytosol from both homozygous and heterozygous rats inhibited microsomal T4-5'-deiodinase activity similarly. Addition of unconjugated bilirubin to liver homogenates resulted in reduction of T3 production in livers from both homozygous and heterozygous rats. Thus the diminished capacity for hepatic conversion of T4 to T3 in homozygous Gunn rats may be due to inhibition of T4-5'-deiodinase activity by high endogenous levels of unconjugated bilirubin.

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