Role of neuromedin B in control of the release of thyrotropin in hypothyroid and hyperthyroid rats.

Rettori, Valéria; Pazos‐Moura, Carmen C.; Moura, Egberto Gaspar de; Polak, Julia M.; McCann, Samuel M.

doi:10.1073/pnas.89.7.3035

Cited by 36 publications

(35 citation statements)

References 6 publications

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“…Other important local TSH-releasing inhibitors, such as the bombesin-like peptide, neuromedin B has its effect regulated by thyroid state. Thyroid hormones act to increase the pituitary neuromedin B, expression (Jones et al 1992, OrtigaCarvalho et al 1996, and probably release, which may explain the higher response to the immunoneutralization of the peptide (Rettori et al 1992). However, it is not known if thyroid hormones are able to modulate leptin or leptin receptor expression at the pituitary.…”

Section: Discussionmentioning

confidence: 96%

Thyroid hormones modulate the endocrine and autocrine/paracrine actions of leptin on thyrotropin secretion

Veiga¹,

Oliveira²,

Curty³

et al. 2004

Journal of Endocrinology

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We investigated the influence of hypo-and hyperthyroidism on the ability of leptin to modulate TSH secretion. Two hours after receiving leptin (8 µg leptin/100 g BW; s.c.), hyperthyroid rats (10 µg thyroxine (T4)/100 g body weight (BW) for 5 days) showed a 1·7-fold increase in serum TSH (P<0·05); in hypothyroid rats, leptin had no effect. Hemi-pituitaries of hyperthyroid rats incubated with 10 9 and 10 7 M leptin showed reductions in TSH release of 40 and 50% respectively (P<0·05); incubation with 1:2000 and 1:500 dilutions of antiserum against leptin resulted in 3-and 4-fold higher TSH release (P<0·05 and P<0·001 respectively). However, in hypothyroid pituitaries leptin or the antiserum had no effect. The results suggest that the in vivo and in vitro responsiveness of TSH to leptin is abolished in hypothyroidism and is preserved in short-term hyperthyroidism, in comparison to previous reports in euthyroidism. In addition, the inhibitory action of pituitary leptin is enhanced in hyperthyroid glands, which may suggest a role for locally produced leptin in the suppression of TSH release associated with hyperthyroidism.

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Section: Discussionmentioning

confidence: 96%

Thyroid hormones modulate the endocrine and autocrine/paracrine actions of leptin on thyrotropin secretion

Veiga¹,

Oliveira²,

Curty³

et al. 2004

Journal of Endocrinology

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“…Each hemipituitary was homogenized in phosphate buffer saline (pH 7 . 6) for measurement of intra-pituitary TSH content (Rettori et al 1992, Moreira et al 1997, Moura et al 2001, Veiga et al 2004, Lisboa et al 2008. Protein content was measured by the Bradford method (Bradford 1976).…”

Section: In Vitro Trh-stimulated Tsh Releasementioning

confidence: 99%

Prolactin inhibition at the end of lactation programs for a central hypothyroidism in adult rat

Bonomo

Lisboa²,

Passos³

et al. 2008

Journal of Endocrinology

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Malnutrition during lactation is associated with hypoprolactinemia and failure in milk production. Adult rats whose mothers were malnourished presented higher body weight and serum triiodothyronine (T 3 ). Maternal hypoprolactinemia at the end of lactation caused higher body weight in adult life, suggesting an association between maternal prolactin (PRL) level and programming of the offspring's adult body weight. Here, we studied the consequences of the maternal PRL inhibition at the end of lactation by bromocriptine (BRO) injection, a dopaminergic agonist, upon serum TSH and thyroid hormones, thyroid iodide uptake, liver mitochondrial a-glycerophosphate dehydrogenase (mGPD), liver and pituitary de-iodinase activities (D1 and/or D2), and in vitro post-TRH TSH release in the adult offspring. Wistar lactating rats were divided into BRO -injected with 1 mg/twice a day, daily for the last 3 days of lactation, and C -control, saline-injected with the same frequency. At 180 days of age, the offspring were injected with 125 I i.p. and after 2 h, they were killed. Adult animals whose mothers were treated with BRO at the end of lactation presented lower serum TSH (K51%), T 3 (K23%), and thyroxine (K21%), lower thyroid 125 I uptake (K41%), liver mGPD (K55%), and pituitary D2 (K51%) activities, without changes in the in vitro post-TRH TSH release. We show that maternal PRL suppression at the end of lactation programs a hypometabolic state in adulthood, in part due to a thyroid hypofunction, caused by a central hypothyroidism, probably due to decreased TRH secretion. We suggest that PRL during lactation can regulate the hypothalamus-pituitary-thyroid axis and programs its function.

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“…Both peptides have been shown to be present in the thyrotrophs, and they have opposite effects on TSH secretion, with SP increasing it while NB and GRP decrease it (26,27,30). Their pituitary levels are modified in opposite directions by thyroid hormone.…”

Section: Discussionmentioning

confidence: 99%

“…NB content (28,29) and action (26,30) at the pituitary gland level are influenced by thyroid status. Hypothyroidism decreases, while thyroid hormone increases pituitary NB and its mRNA content (28,29).…”

Section: Introductionmentioning

confidence: 99%

Interaction between substance P and gastrin-releasing peptide on thyrotropin secretion by rat pituitary in vitro

Moura

Santos

et al. 1999

Braz J Med Biol Res

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The effect of substance P (SP) on thyrotropin (TSH) secretion is controversial. In this study we evaluated the effect of SP on TSH secretion by hemipituitaries of 3-month-old Wistar rats in vitro and its interaction with gastrin-releasing peptide (GRP) at equimolar concentrations (1 µM and 10 µM). TSH release was measured under basal conditions and 30 min after incubation in the absence or presence of SP, GRP or both peptides. Pituitary TSH content was also measured in the pituitary homogenate after incubation. SP at both concentrations caused a significant (P<0.05) increase in TSH secretion compared with all other groups, which was approximately 60% (1 µM) and 85% (10 µM) higher than that of the control group (23.3 ± 3.0 ng/ml). GRP at the lower concentration did not produce a statistically significant change in TSH secretion, whereas at the concentration of 10 µM it produced a 50% reduction in TSH. GRP co-incubated with substance P completely blocked the stimulatory effect of SP at both concentrations. Pituitary TSH content decreased in the SP-treated group compared to controls (0.75 ± 0.03 µg/hemipituitary) at the same proportion as the increase in TSH secretion, and this effect was also blocked when GRP and SP were co-incubated. In conclusion, in an in vitro system, SP increased TSH secretion acting directly at the pituitary level and this effect was blocked by GRP, suggesting that GRP is more potent than SP on TSH secretion, and that this inhibitory effect could be the predominant effect in vivo.

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Role of neuromedin B in control of the release of thyrotropin in hypothyroid and hyperthyroid rats.

Cited by 36 publications

References 6 publications

Thyroid hormones modulate the endocrine and autocrine/paracrine actions of leptin on thyrotropin secretion

Thyroid hormones modulate the endocrine and autocrine/paracrine actions of leptin on thyrotropin secretion

Prolactin inhibition at the end of lactation programs for a central hypothyroidism in adult rat

Interaction between substance P and gastrin-releasing peptide on thyrotropin secretion by rat pituitary in vitro

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