Correlation between the number of thyroliberin binding sites, the tumour size and the plasma prolactin level in human prolactin-secreting adenomas

Dafniet, M. Le; Pagésy, Patrick; Brandi, A. M.; Racadot, J; Peillon, F

doi:10.1530/acta.0.1080464

Cited by 6 publications

(8 citation statements)

References 4 publications

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“…A positive correlation (p = 0.729, p < 0.001) could be demonstrated between the plasma PRL level and the number of TRH-binding sites (table 1) [7], This correlation might indicate a possible implication of the TRH stimulatory control of PRL in prolactinomas. Combined with a possible defect in the dopaminergic control it could be part of the mechanism inducing hyperprolactinemia.…”

Section: Trh Receptorsmentioning

confidence: 74%

Receptors and Neurohormones in Human Pituitary Adenomas

Peillon

Dafniet²,

Garnier³

et al. 1989

Horm Res

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In order to go further into the pathogenesis of human pituitary adenomas, we studied receptors for neurohormones (thyroliberin, TRH; dopamine, DA; somatostatin, SRIH), for estradiol and epidermal growth factor (EGF) thought to influence hormone secretion and/or cell growth. The following results were obtained: (1) the receptors listed above, with the exception of EGF receptors in the adenomas, are present in normal pituitary tissue and in prolactin (PRL)- and growth hormone (GH)-secreting adenomas; (2) they are functional and their affinities are not different in normal or tumoral tissues; (3) their density is variable and depends on the type of secreting adenoma (GH or PRL), the size of the tumor and the plasma level of the hormone which is secreted, and (4) in nonsecreting adenomas, only TRH receptors are found with characteristics identical to those observed in secreting adenomas. We also showed that TRH is contained in normal and tumoral pituitary tissues. TRH and SRIH are released in vitro from adenomatous cells in large amounts, suggesting their possible synthesis by the pituitary. In both cases a local regulation is observed. TRH release is stimulated in the presence of DA while SRIH is inhibited in the presence of TRH. This neuropeptide release may be implicated in the pituitary hormone regulation through a paracrine or an autocrine mechanism. Thus, the neurohormone receptors found in pituitary adenomas should be dependent on a more complex regulation than it has been envisaged till now.

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Section: Trh Receptorsmentioning

confidence: 74%

Receptors and Neurohormones in Human Pituitary Adenomas

Peillon

Dafniet²,

Garnier³

et al. 1989

Horm Res

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“…The latter are characterized by non-suppressibility of plasma TSH values by elevated thyroid hormone concentrations and generally absence of TSH response to TRH, suggesting a relative autonomy of tumoral thyrotropic cells. We have demonstrated the presence of TRH binding sites on cell membranes of human PRL and GH-secreting adenomas (2,3), as well as of non-secreting adenomas and normal anterior pituitaries (4). By contrast, we have been unable to detect such TRH receptors in three cases of human TSH-secreting adenomas associated with hyperthyroidism (5,6).…”

Section: Paris Francementioning

confidence: 67%

Thyrotropin-releasing hormone (TRH) binding sites and thyrotropin response to TRH are regulated by thyroid hormones in human thyrotropic adenomas

Dafniet

Brandi²,

Kujas³

et al. 1994

European Journal of Endocrinology

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In order to see whether, in thyrotropic adenomas with thyrotoxicosis, plasma thyroid hormones regulate the thyrotropin-releasing hormone (TRH) binding sites and the thyrotropin (TSH) response to TRH, we investigated: the presence of TRH binding sites in two cases of thyrotropic adenomas associated with hyperthyroidism and in one case of thyrotropic adenoma secondary to thyroid failure: and the in vitro effect, in a perifusion system, of triiodothyronine (T3) on the response of TSH to TRH in three cases of TSH-secreting adenomas associated with hyperthyroidism. The TRH binding sites were absent in the adenomas associated with high levels of circulating thyroid hormones, whereas they were present in the adenoma secondary to primary thyroid failure (Kd = 47 nmol/l, Bmax = 40 nmol/kg membrane proteins). In vitro, the three adenomas spontaneously released TSH in the perifusion medium (1.49 +/- 0.06 (mean +/- SEM), 7.25 +/- 0.12 and 16.73 +/- 0.36 mIU.l-1 x 10(6) cells-1 x 2 min-1) and exhibited an ample TSH response to 10(-7) mol/l TRH pulses. In two cases, tumoral secretion of fragments was compared with those of fragments maintained since the time of surgical removal in the presence of 10(-8) mol/lT3. The TSH responses to TRH were abolished in the presence of T3 in these two cases. We conclude that thyrotropic adenomas associated with hyperthyroidism are still controlled in vivo by T3. In particular, T3 regulates the TSH response to TRH, probably via a down-regulation of the TRH binding sites.

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“…The mean TRH concentration in the 16 prolactinomas was similar to that we recently found in normal human pituitaries (17), although the values varied more. The individual TRH concentrations were not correlated with the plasma PRL levels of the patients or the size of the tumor and, consequently, the number of TRH-binding sites (12). The amounts of DA in the normal human pituitaries were in the same range as those in rat pituitaries (23), and DA was almost undetectable in the prolactinomas.…”

Section: Discussionmentioning

confidence: 79%

“…A decrease in DA and/or an increase in TRH released from the hypothalamus and internalized in the pituitary cells could explain our results. In favor of this explanation are the findings of fewer DA-binding sites in prolactinomas than in normal pituitaries (6) and high levels of TRHbinding sites in prolactinomas (12). The absence of 3,4-dihydroxyphenylacetic acid in the tumors as well as in normal pituitary tissue does not suggest increased tissue DA metabolism.…”

Section: Discussionmentioning

confidence: 97%

“…In particular, prolactinomas have functional receptors for TRH (11), and there is a positive correlation among plasma PRL levels, tumor size, and the number of TRH-binding sites in the tumors (12). Thus, one could envisage that both hormone hypersecretion and cell proliferation would result from an imbalance between DA inhibitory and TRH stimulatory regulation rather than a defect in dopaminergic inhibition alone.…”

mentioning

confidence: 99%

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Altered Balance between Thyrotropin-Releasing Hormone and Dopamine in Prolactinomas and Other Pituitary Tumors Compared to Normal Pituitaries

Dafniet

Blumberg-Tick²,

Gozlan³

et al. 1989

The Journal of Clinical Endocrinology & Metabolism

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We measured TRH and dopamine (DA) concentrations in prolactinomas and other pituitary tumors in order to further understand the roles of these two factors in the hormone hypersecretion and growth of these tumors. The mean TRH concentration (by RIA) in 16 prolactinomas was 247 +/- 92 (+/- SE) fmol/mg cell protein (range, 10-1297), near that found in normal pituitary tissue. The prolactinoma TRH content did not correlate with the patient's tumor size or plasma PRL level. By contrast, DA assayed by high pressure liquid chromatography was present in normal pituitary tissue (7.3 +/- 3.5 pmol/mg cell protein), but was very low or undetectable in the prolactinomas (23 fmol/mg cell protein or less). 3,4-Dihydroxyphenylacetic acid, also assayed by high pressure liquid chromatography, was undetectable in both normal pituitary tissue and prolactinomas. This imbalance between TRH and DA content also was found in GH-secreting and nonsecreting adenomas. The TRH content in 18 GH-secreting tumors (24 +/- 6 fmol/mg) was considerably lower than that in the prolactinomas (P less than 0.001). In 8 nonsecreting adenomas, the mean TRH concentration was 109 +/- 28 fmol/mg, about half of that in the prolactinomas. In those 2 types of adenomas, DA also was nearly undetectable (less than or equal to 73 fmol/mg cell protein). We conclude that the imbalance between TRH and DA contents in prolactinomas compared to those in normal pituitary tissue might participate in the mechanisms leading to hypersecretion of PRL and the growth of all types of pituitary adenomas.

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Correlation between the number of thyroliberin binding sites, the tumour size and the plasma prolactin level in human prolactin-secreting adenomas

Cited by 6 publications

References 4 publications

Receptors and Neurohormones in Human Pituitary Adenomas

Receptors and Neurohormones in Human Pituitary Adenomas

Thyrotropin-releasing hormone (TRH) binding sites and thyrotropin response to TRH are regulated by thyroid hormones in human thyrotropic adenomas

Altered Balance between Thyrotropin-Releasing Hormone and Dopamine in Prolactinomas and Other Pituitary Tumors Compared to Normal Pituitaries

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