Rapid alteration in circulating free thyroxine modulates pituitary type II 5' deiodinase and basal thyrotropin secretion in the rat.

Abend, Susan; Fang, Shiuh-Bin; Alex, Sharon; Braverman, Lewis E.; Leonard, Jack L.

doi:10.1172/jci115392

Cited by 30 publications

(14 citation statements)

References 29 publications

(28 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Despite one study [26] suggesting that both T4 and T3 might act directly on the pituitary gland to inhibit TSH secretion, most authors consider that T3, more so than T4, exerts its inhibitory effect on TSH secretion. This could explain why the TSH in the HISe group was lower at the end of the trial, potentially due to a more potent inhibitory effect of T3 on the pituitary gland.…”

Section: Selenium and Iodine Status Of The Cowsmentioning

confidence: 99%

Effect of a combined iodine and selenium supplementation on I and Se status of cows and their calves

Guyot

Oliveira

Ramery

et al. 2011

Journal of Trace Elements in Medicine and Biology

View full text Add to dashboard Cite

Section: Selenium and Iodine Status Of The Cowsmentioning

confidence: 99%

Effect of a combined iodine and selenium supplementation on I and Se status of cows and their calves

Guyot

Oliveira

Ramery

et al. 2011

Journal of Trace Elements in Medicine and Biology

View full text Add to dashboard Cite

“…Recently, it was demonstrated that T4 also appears to have a direct effect on TSH suppression (Abend et al 1991). Triac also suppressed TSH secretion in humans (Mechelany et al 1991, Sherman & Ladenson 1992, Bracco et al 1993) but exhibited substantial thyromimetic effects.…”

Section: Administration Of T2 In Rat Pituitary Fragmentsmentioning

confidence: 99%

3,5-Di-iodo-l-thyronine suppresses TSH in rats in vivo and in rat pituitary fragments in vitro

Horst¹,

Harneit²,

Seitz³

et al. 1995

Journal of Endocrinology

View full text Add to dashboard Cite

3,5-Di-iodo-L-thyronine (T2) is a naturally occurring metabolite of thyroxine (T4). Contrary to earlier findings, T2 has recently been shown to have rapid effects in rat liver and in mononuclear blood cells. In the experiments described here, T2 was tested to determine whether it has a TSH suppressive effect in rats in vivo and in rat pituitary fragments in vitro. In experiments over 2 weeks in rats in vivo, low doses of T2 (20-200 micrograms/100 g body weight per day) had no significant influence on body and organ weights, but significantly decreased TSh and T4 serum concentrations. At 200 micrograms/100 g per day, T2 suppressed TSH to 43% and T4 to 29% of control levels. At 1-15 micrograms/100 g per day, 3,5,3'-tri-iodo-L-thyronine (T3), used as a comparison to T2, had significant effects on TSH and T4 levels, and also on body weight. Fifteen micrograms T3/100 g per day decreased TSH to 44%, T4 to 25%, and body weight to 59% of control levels. In experiments over 3 months in rats in vivo, a low dose (25 micrograms/100 g per day) of T2 suppressed TSH to 60% and T4 to 57% of control levels and had no significant influence on other parameters. Conversely, 0.1 microgram/100 g per day T3 had significant effects on body and organ weights as well as pellet intake, but a less pronounced TSH suppressive effect: TSH concentrations were unchanged and T4 concentrations were down to 80% of control values.(ABSTRACT TRUNCATED AT 250 WORDS)

show abstract

“…Nonetheless, the intrinsic homeostatic nature of D2 weakens the argument for its proposed major role in the TSH feedback mechanism (10). It is well known that low-serum T 4 increases D2 activity and that high T 4 concentrations do the opposite (11).…”

mentioning

confidence: 99%

Atypical Expression of Type 2 Iodothyronine Deiodinase in Thyrotrophs Explains the Thyroxine-Mediated Pituitary Thyrotropin Feedback Mechanism

et al. 2006

View full text Add to dashboard Cite

T(4), the main product of thyroid secretion, is a critical signal in plasma that mediates the TSH-negative feedback mechanism. As a prohormone, T(4) must be converted to T(3) to acquire biological activity; thus, type 2 iodothyronine deiodinase (D2) is expected to play a critical role in this feedback mechanism. However, the mechanistic details of this pathway are still missing because, counterintuitively, D2 activity is rapidly lost in the presence of T(4) by a ubiquitin-proteasomal mechanism. In the present study, we demonstrate that D2 and TSH are coexpressed in rat pituitary thyrotrophs and that hypothyroidism increases D2 expression in these cells. Studies using two murine-derived thyrotroph cells, TtT-97 and TalphaT1, demonstrate high expression of D2 in thyrotrophs and confirm its sensitivity to negative regulation by T(4)-induced proteasomal degradation of this enzyme. Despite this, expression of the Dio2 gene in TalphaT1 cells is higher than their T(4)-induced D2 ubiquitinating capacity. As a result, D2 activity and net T(3) production in these cells are sustained, even at free T(4) concentrations that are severalfold above the physiological range. In this system, free T(4) concentrations and net D2-mediated T(3) production correlated negatively with TSHbeta gene expression. These results resolve the apparent paradox between the homeostatic regulation of D2 and its role in mediating the critical mechanism by which T(4) triggers the TSH-negative feedback.

show abstract

Rapid alteration in circulating free thyroxine modulates pituitary type II 5' deiodinase and basal thyrotropin secretion in the rat.

Cited by 30 publications

References 29 publications

Effect of a combined iodine and selenium supplementation on I and Se status of cows and their calves

Effect of a combined iodine and selenium supplementation on I and Se status of cows and their calves

3,5-Di-iodo-l-thyronine suppresses TSH in rats in vivo and in rat pituitary fragments in vitro

Atypical Expression of Type 2 Iodothyronine Deiodinase in Thyrotrophs Explains the Thyroxine-Mediated Pituitary Thyrotropin Feedback Mechanism

Contact Info

Product

Resources

About