The influence of thyroid hormone status on the hypothalamo-hypophyseal-growth-hormone axis

Jones, P J; Burrin, JM; Ghatei, M.A.; O'Halloran, D.J.; Bloom, S.R.

doi:10.1016/0167-0115(89)90144-4

Cited by 21 publications

(35 citation statements)

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“…Other laboratories have recently reported that hypothalamic GRFmRNA levels in rats were increased in hypothyroidism (26,27,61 ) and decreased in hyperthyroidism (61). This negative relationship between GRF mRNA and thyroid function is similar to that which we found between GRF secretion and serum T4.…”

Section: Resultssupporting

confidence: 78%

Thyroid hormone modulation of the hypothalamic growth hormone (GH)-releasing factor-pituitary GH axis in the rat.

Miki¹,

Ono²,

Hizuka³

et al. 1992

J. Clin. Invest.

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Both thyroid hormone and hypothalamic growth hormone (GH)-releasing factor (GRF) facilitate pituitary somatotroph function. However, the pathophysiological role of thyroid hormone in GRF secretion is less well understood. Thyrotoxicosis, induced by administration of thyroxine (T4) in rats, inhibited both pituitary GH levels and immunoreactive GRF secretion from incubated hypothalamus. At the highest dose of T4 given for 12 d, GRF secretion and pituitary GH decreased by 50 and 39%, respectively. Hypothyroidism induced by thyroidectomy (T.) enhanced GRF secretion approximately twofold while depleting pituitary GH by > 99%. Both, of these hypothalamic and pituitary effects were reversed by replacement of T4 but not human GH for 7 or 14 d. Human GH was as potent as T4 in restoring decreased body weight gains or serum insulin-like growth factor-i levels in T. rats. These results indicate that at both physiological and pathological concentrations in serum, thyroid hormone acts as an inhibitory modulator of GRF secretion, probably not involving a feedback mechanism through GH. A biphasic effect of thyroid hormone on pituitary GH levels appears to derive from the difference in primary target tissues of hyper-and hypothyroidism, the hypothalamus and the pituitary, respectively. (J. Clin. Invest. 1992.90:113-120.)

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Section: Resultssupporting

confidence: 78%

Thyroid hormone modulation of the hypothalamic growth hormone (GH)-releasing factor-pituitary GH axis in the rat.

Miki¹,

Ono²,

Hizuka³

et al. 1992

J. Clin. Invest.

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“…Previous studies have raised the possibility that T 2 may have extra-nuclear effects, independent of classical nuclear TRs (Horst et al 1989, Kvetny 1992, Lanni et al 1993, Goglia et al 1994. Both GH and TSH mRNA levels can be regulated at a posttranscriptional level by T 3 (Jones et al 1990, Krane et al 1991. Similarly, ME synthesis in the liver is regulated at both transcriptional and posttranscriptional levels (Dozin et al 1986).…”

Section: Discussionmentioning

confidence: 99%

3,5-Diiodo-L-thyronine (T2) has selective thyromimetic effects in vivo and in vitro

Ball¹,

Sokolov²,

Ww³

1997

Journal of Molecular Endocrinology

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Recent data have suggested that the iodothyronine, 3,5-diiodo-l-thyronine (T 2 ), has selective thyromimetic activity. In vivo, T 2 has been shown to suppress TSH levels at doses that do not produce significant peripheral manifestations of thyroid hormone activity. Furthermore, T 2 has been shown to produce smaller increments in peripheral indices of thyroid status than does T 3 , when doses resulting in equivalent suppression of circulating TSH are compared. We have assessed the selective thyromimetic activity of T 2 in vivo and in vitro, and performed in vitro studies to assess the potential molecular basis for these selective properties. T 2 was 100-fold less potent than T 3 in stimulating GH mRNA levels in GH 3 cells. In contrast, the iodothyronines were almost equivalent in their ability to downregulate TR 2 mRNA levels in this cell line. Both 3,3 -diiodo--thyronine and thyronine exhibited no significant thyromimetic effects on either process. In vivo, doses of T 2 and T 3 that were equivalent in their induction of hepatic malic enzyme (ME) mRNA did not produce equivalent suppression of circulating TSH, with T 2 being only 27% as effective as T 3 . T 2 was up to 500-fold less potent than T 3 in displacing [125 I]-T 3 from in vitro translated specific nuclear receptors (TRs) and GH 3 cell nuclear extracts. Electrophoretic mobility shift assays, assessing the ability of T 2 to produce dissociation of TR 1 homodimers from inverted palindrome T 3 response elements, indicated that T 2 was also 1000-fold less potent than T 3 in this respect. These data confirm that T 2 has significant thyromimetic activity, and that this activity is selective both in vivo and in vitro. However, there are no data to support a selective central effect, T 2 being relatively more potent in stimulating hepatic ME mRNA than in suppression of TSH in vivo. The basis for this differential thyromimetic activity is not selective affinity of the different TR isoforms for T 2 , or divergent properties of T 2 in competitive binding and functional assays in vitro.

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“…The molecular mechanism(s) by which activation of D 2 DA receptors destabilizes PRL mRNA half-life remains to be clarified. Alterations in one or more of the following mechanisms may be involved: (i) the length of the PRL mRNA poly (A) tail (Diamond & Goodman, 1985, Jones et al 1990), (ii) the effect on the destabilizing sequence elements, such as AU-rich elements, if they exist (Shaw & Kamen 1986), or (iii) the RNA-binding proteins which play a major role in regulating the mRNA half-life (Staton et al 2000).…”

Section: Discussionmentioning

confidence: 99%

Dopaminergic regulation of avian prolactin gene transcription

Kahtane

Chaiseha

Halawani

2003

Journal of Molecular Endocrinology

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It is well documented that prolactin (PRL) release and PRL gene expression in birds are controlled by the tonic stimulation of hypothalamic vasoactive intestinal peptide (VIP). However, there is good evidence that dopamine (DA) exerts both stimulatory (at the hypothalamic level) and inhibitory (at the pituitary level) effects on PRL secretion. The interactions between VIP and DA in the regulation of PRL gene transcription are not known. This study was designed to examine the effects of a D 2 DA receptor agonist (D 2 AG; R(−)-propylnorapomorphine HCl) on basal and VIP-stimulated PRL gene transcription rate, PRL mRNA steady-state levels, PRL mRNA stability and PRL release from cultured turkey anterior pituitary cells. The D 2 AG (10 −10 M) completely inhibited the stimulatory effect of VIP (10 −7 M) upon nascent PRL mRNA as determined utilizing a nuclear run-on transcription assay. To examine further the effect of the D 2 AG on PRL mRNA post-transcriptional events, anterior pituitary cells were treated with different concentrations of D 2 AG (10 −12 -10 −4 M). Semi-quantitative RT-PCR and RIA were performed to determine the levels of PRL mRNA and PRL content in the medium respectively. The results show that D 2 AG inhibited VIP-stimulated PRL mRNA steady-state levels as well as basal and VIP-stimulated PRL release, effects which were diminished by the D 2 DA receptor antagonist, S(−)-eticlopride HCl (10 −10 M). Actinomycin D (5 µg/ml), an inhibitor of mRNA synthesis, was used to assess the effect of D 2 AG on PRL mRNA stability in response to VIP. The stimulatory effect of VIP on PRL mRNA stability was completely negated by the D 2 AG (from a half-life of 53·0±2·3 h in VIP-treated cells to 25·5±1·6 h in D 2 AG+VIP-treated cells, P≤0·05). These results support the hypothesis that VIP and DA play a major role in the regulation of PRL gene expression in avian species, at both the transcriptional and post-transcriptional levels. In addition, these findings suggest that the DAergic system inhibits PRL release and synthesis by antagonizing VIP at the pituitary level via D 2 DA receptors.

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The influence of thyroid hormone status on the hypothalamo-hypophyseal-growth-hormone axis

Cited by 21 publications

References 0 publications

Thyroid hormone modulation of the hypothalamic growth hormone (GH)-releasing factor-pituitary GH axis in the rat.

Thyroid hormone modulation of the hypothalamic growth hormone (GH)-releasing factor-pituitary GH axis in the rat.

3,5-Diiodo-L-thyronine (T2) has selective thyromimetic effects in vivo and in vitro

Dopaminergic regulation of avian prolactin gene transcription

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