On the enterohepatic cycle of triiodothyronine in rats; importance of the intestinal microflora

Herder, Wouter W. de; Hazenberg, M. P.; Pennock-Schröder, A.M.; Oosterlaken, A.C.; Rutgers, Marja; Visser, Theo J.

doi:10.1016/0024-3205(89)90179-3

Cited by 33 publications

(18 citation statements)

References 25 publications

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“…Active T 3 may then be recovered from T3S through the action of sulfatases in tissues where hormone action is required or by bacterial sulfatases in the intestine. We have indeed demonstrated that bacterial sulfatases are important for the resorption of T 3 following biliary excretion of T3S [40][41][42]. Furthermore, significant hydrolysis of T3S has been detected in liver and brain microsomes in humans and rats [43].…”

Section: Possible Role Of Iodothyronine Suifationmentioning

confidence: 95%

The role of sulfation in thyroid hormone metabolism

Visser

Buuren

Rutgers

et al. 1990

Trends in Endocrinology & Metabolism

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The type 1 iodothyronine deiodinase (1D-I) in liver and kidney converts the prohormone thyroxine ('1"4) by outer ring deiodination (ORD) to bioactive 3,3',5-triiodothyronine (T3) or by inner ring deiodination (IRD) to inactive 3,3',5-"triiodothronine (rT3), while it also catalyzes the IRD of T3 and the ORD of rT 3, with the latter as the preferred substrate. Sulfation of the phenolic hydroxyl group blocks the ORD of T 4, while it strongly stimulates the IRD of both T 4 and T3, indicating that sulfation is an important step in the irreversible inactivation of thyroid hormone. This review summarizes recent studies concerning this interaction between sulfation and deiodination of iodothyronines, the characterization of iodothyronine sulfotransferase activities, the measurement of iodothyronine sulfates in humans and animals, and the possible physiological importance of iodothyronine sulfation.

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Section: Possible Role Of Iodothyronine Suifationmentioning

confidence: 95%

The role of sulfation in thyroid hormone metabolism

Visser

Buuren

Rutgers

et al. 1990

Trends in Endocrinology & Metabolism

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“…For instance, thyroid horm ones (T 4 and T 3 ) are known to be enterohepatically circulated (7,29,36). Therefore, increased enterohepatic circulation could play a role in m aintaining serum T 3 .…”

Section: Effects Of Microsomal Enzyme Inducers On Outer-ring Deiodinamentioning

confidence: 99%

Effects of Microsomal Enzyme Inducers on Thyroid Follicular Cell Proliferation and Thyroid Hormone Metabolism

Klaassen

Hood

2001

Toxicol Pathol

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The effects of microsomal enzyme inducers on thyroid hormone homeostasis and the thyroid gland are of concern. We have investigated the effects of microsomal enzyme inducers on thyroid follicular cell proliferation and thyroid hormone metabolism in rats. We have shown that small increases in serum TSH can result in large increases in thyroid follicular cell proliferation. Furthermore, only those microsomal enzyme inducers that increase serum TSH--that is, phenobarbital (PB) and pregnenolone-16alpha-carbonitrile (PCN)-increase thyroid follicular cell proliferation, whereas those microsomal enzyme inducers that do not increase serum TSH--that is, 3-methylcholanthrene (3MC) and Aroclor 1254 (PCB)-do not increase thyroid follicular cell proliferation. Deiodination does not appear to be the reason why serum T3 concentrations are maintained in microsomal enzyme inducer-treated rats. We have also shown that those microsomal enzyme inducers that increase serum TSH increase T3 UDP-glucuronosyltransferase (UGT) activity, whereas those microsomal enzyme inducers that do not increase serum TSH do not increase T3 UGT activity. This finding suggests that induction of T3 glucuronidation, rather than T4 glucuronidation, mediates increases in serum TSH of microsomal enzyme inducer treated rats.

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“…Iodothyronine glucuronides are excreted in bile, but this is not an irreversible route for thyroid hormone disposal. The glucuronides are extensively deconjugated in the intestinal lumen, in particular by 13-glucuronidases of bacterial origin, and part of the liberated iodothyronines is reabsorbed (Hazenberg et al, 1988;De Herder et al, 1989;Rutgers et al, 1989). Because of this enterohepatic circulation, the intestinal content represents a large pool of thyroid hormone (Nguyen et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

Effects of thyroid status and thyrostatic drugs on hepatic glucuronidation of lodothyronines and other substrates in rats

Visser

Kaptein

Gijzel

et al. 1996

Endocr

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Glucuronidation of iodothyronines in rat liver is catalyzed by at least three UDP-glucuronyltransferases (UGTs): bilirubin UGT, phenol UGT, and androsterone UGT. Bilirubin and phenol UGT activities are regulated by thyroid hormone, but the effect of thyroid status on hepatic glucuronidation of iodothyronines is unknown. We examined the effects of hypothyroidism induced by treatment of rats with propylthiouracil (PTU) or methimazole (MMI) or by thyroidectomy as well as the effects of T4-induced hyperthyroidism on the hepatic UGT activities for T4, T3, bilirubin, p-nitrophenol (PNP), and androsterone. Bilirubin UGT activity was increased in MMI-or PTU-induced hypothyroid and thyroidectomized rats, and decreased in hyperthyroid animals. T4 and, to a lesser extent, T3 UGT activities were increased in MMI-or PTU-induced hypothyroid rats, and T4 but not T3 glucuronidation also showed a significant increase in thyroidectomized rats. T4 but not T3 UGT activity was slightly decreased in hyperthyroid rats. While PNP UGT activity was decreased in thyroidectomized rats and increased in hyperthyroid animals, it was also markedly increased by MMI and slightly increased by PTU-induced hypothyroidism. In T4-substituted rats, MMI did not affect T4, T3, bilirubin and androsterone UGT activities but again strongly induced PNP UGT activity, indicating that this represented a direct induction of PNP UGT by the drug independent of its thyrostatic action. Androsterone UGT activity was hardly affected by thyroid status. Our results suggest a modest, negative control of the hepatic glucuronidation of thyroid hormone by

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On the enterohepatic cycle of triiodothyronine in rats; importance of the intestinal microflora

Cited by 33 publications

References 25 publications

The role of sulfation in thyroid hormone metabolism

The role of sulfation in thyroid hormone metabolism

Effects of Microsomal Enzyme Inducers on Thyroid Follicular Cell Proliferation and Thyroid Hormone Metabolism

Effects of thyroid status and thyrostatic drugs on hepatic glucuronidation of lodothyronines and other substrates in rats

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