Metabolism of reverse triiodothyronine by isolated rat hepatocytes.

Rooda, Sebo Jan Eelkman; Loon, M A van; Tj, Visser

doi:10.1172/jci113014

Cited by 26 publications

(6 citation statements)

References 31 publications

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“…These results are in excellent agreement with in vitro observations of the rapid metabolism of rT3 and 3,3'-T2 by isolated rat hepatocytes (Otten et al 1983;Eelkman Rooda et al 1987). In case of rT3 this is readily explained by the known sub¬ strate specificity of the type I deiodinase.…”

Section: Discussionsupporting

confidence: 88%

“…In rat hepatocytes, 3,3'-T2 is rapidly metabolized by successive sulphation and type I deiodination of the outer ring (Otten et al 1983). The high rate of 3,3'-T2 sulphation explains why little 3,3'-T2 formation is observed if rT3 is incubated with rat hepatocytes (Eelkman Rooda et al 1987). These findings suggest that rT3 and 3,3'-T2 produced in the human liver are further metabolized before being released into the circulation.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Handling of iodothyronines by the liver and kidney in patients with chronic liver disease

Bauer¹,

Wilson²,

Lamberts³

et al. 1987

Acta Endocrinologica

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Possible arterio-venous gradients of T4, T3, rT3 and 3,3'-diiodothyronine (3,3'-T2) across the liver and the kidneys were measured in 9 patients with varying degrees of liver failure undergoing diagnostic catheterization. Plasma iodothyronine levels were measured in peripheral, hepatic and renal veins before and at 10-min intervals until 60 min after iv injection of 400 \ of TRH. In 2 patients estimated hepatic plasma flow and effective renal plasma flow were determined as well. In these 2 patients, no significant differences between iodothyronine levels in arterial and peripheral venous plasma were found. T4 and T3 levels were not -217.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Handling of iodothyronines by the liver and kidney in patients with chronic liver disease

Bauer¹,

Wilson²,

Lamberts³

et al. 1987

Acta Endocrinologica

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“…In order to investigate whether the lipid-lowering effects of T 3 on FaO cells might depend on local, intracellular T 3 -to-T 2 conversion via deiodinase activities, the experiments with T 3 were repeated in the presence of PTU, an inhibitor of type I deiodinase, that is known to be expressed in rat liver hepatocytes (Rooda et al 1987). The effects of T 3 were unchanged by PTU (Fig.…”

Section: Effects Of Iodothyronines On Lipid Accumulationmentioning

confidence: 99%

Non-receptor-mediated actions are responsible for the lipid-lowering effects of iodothyronines in FaO rat hepatoma cells

Grasselli

Voci

Canesi

et al. 2011

Journal of Endocrinology

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Iodothyronines influence lipid metabolism and energy homeostasis. Previous studies demonstrated that 3,5-L-diiodothyronine (T 2 ), as well as 3,3 0 ,5-L-triiodothyronine (T 3 ), was able to both prevent and reverse hepatic steatosis in rats fed a high-fat diet, and this effect depends on a direct action of iodothyronines on the hepatocyte. However, the involvement of thyroid hormone receptors (TRs) in mediating the lipid-lowering effect of iodothyronines was not elucidated. In this study, we investigated the ability of T 2 and T 3 to reduce the lipid overloading using the rat hepatoma FaO cells defective for functional TRs. The absence of constitutive mRNA expression of both TRa1 and TRb1 in FaO cells was verified by RT-qPCR. To mimic the fatty liver condition, FaO cells were treated with a fatty acid mixture and then exposed to pharmacological doses of T 2 or T 3 for 24 h. Lipid accumulation, mRNA expression of the peroxisome proliferator-activated receptors (PPAR-a, -g, -d) the acyl-CoA oxidase (AOX), and the stearoyl CoA desaturase (SCD1), as well as fuel-stimulated O 2 consumption in intact cells, were evaluated. Lipid accumulation was associated with an increase in triacylglycerol content, PPARg mRNA expression, and a decrease in PPARd and SCD1 mRNA expression. The addition of T 2 or T 3 to lipid-overloaded cells resulted in i) reduction in lipid content; ii) downregulation of PPARa, PPARg, and AOX expression; iii) increase in PPARd expression; and iv) stimulation of mitochondrial uncoupling. These data demonstrate, for the first time, that in the hepatocyte, the lipid-lowering actions of both T 2 and T 3 are not mediated by TRs.

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“…The reaction was started by adding the cytosol and was stopped by adding 0.8 mL 0.1 N HCl to the reaction mixture. The formation of iodothyronine sulfate was analyzed using Sephadex LH-20 chromatography on a mini-column (bed volume, 0.75 mL), pre-equilibrated with 0.1 N HCl, as described (Rooda et al, 1987). Free iodine, sulfated iodothyronines, and nonsulfated iodothyronines were eluted successively using six 1 mL aliquots of 0.1 N HCl, ten 1 mL aliquots of distilled water and six 1 mL aliquots of 0.2 M ammonia/ethanol (1/1, vol/vol) (Rutgers et al, 1987).…”

Section: Assay Of Iodothyronine Sult Activitymentioning

confidence: 99%

Characterization of iodothyronine sulfotransferase activity in the cytosol of Rana catesbeiana tadpole tissues

Rahman

Yamauchi

2010

General and Comparative Endocrinology

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We have investigated the sulfation of thyroid hormones (THs) in the cytosol from Rana catesbeiana tadpole tissues. Sulfation of 3,3',5-triiodothyronine (T(3)) by the liver cytosol, which was dependent on protein amount, incubation time, and temperature, suggested the presence of TH sulfotransferases (SULTs) in the liver. The apparent Michaelis-Menten constant (K(m)) of the liver cytosol was 0.22 microM for T(3), and the apparent maximum velocity (V(max)) of the liver cytosol was 7.65 pmol/min/mg protein for T(3). Iodothyronine sulfating activity in the liver cytosol was increased in tadpoles at premetamorphic (stages IX-X) and metamorphic climax (stage XX) stages, and in adult frogs. The substrate preference of iodothyronine sulfation for the liver cytosol from tadpoles (stage X) was: 3,3',5'-triiodothyronine>T(3)>3,3',5,5'-tetraiodothyroacetic acid>3,3',5-triiodothyroacetic acid, T(4), 3-iodothyronine>3,5-diiodothyronine. Several halogenated phenols were potent inhibitors (IC(50)=0.15-0.21 microM). The substrate preference for T(3) was gradually lost by the onset of metamorphic climax stages. These enzymatic characteristics of iodothyronine sulfation in the liver cytosol from tadpoles resembled those of mammalian phenol SULTs, except that the tadpole cytosol had a higher affinity (one or two orders of magnitude) for T(3) than mammalian SULTs. These results suggested that an enzyme homologous to mammalian phenol SULT (SULT1) may be involved in TH metabolism in tadpoles.

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Metabolism of reverse triiodothyronine by isolated rat hepatocytes.

Cited by 26 publications

References 31 publications

Handling of iodothyronines by the liver and kidney in patients with chronic liver disease

Handling of iodothyronines by the liver and kidney in patients with chronic liver disease

Non-receptor-mediated actions are responsible for the lipid-lowering effects of iodothyronines in FaO rat hepatoma cells

Characterization of iodothyronine sulfotransferase activity in the cytosol of Rana catesbeiana tadpole tissues

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