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Biomedical subjects

C C Pazos-Moura

Publications and source records attributed to C C Pazos-Moura.

At least 19 recordsLinked to original sources
PubMed2006

Leptin acute modulation of the 5'-deiodinase activities in hypothalamus, pituitary and brown adipose tissue of fed rats.

Leptin and thyroid hormones (TH) have the ability to increase energy expenditure. Biological effects of TH are dependent on thyroxine (T4) to triiodothyronine (T3) conversion by deiodinase type 1 (D1) and type 2 (D2). Leptin has been shown to stimulate the hypothalamus-pituitary-thyroid axis and, also, to modulate 5'-deiodinases in different tissues, depending on energetic status of animals. Here, we examined the acute effects of leptin on hypothalamic, pituitary and BAT D2 and pituitary D1 activities. Male fed rats received a single subcutaneous injection of saline or leptin (8 microg/100 g BW) and sacrificed 2 hours later. Leptin promoted an important decrease in hypothalamic D2 (55% reduction, p <0.001) with no changes in pituitary D2, in concomitance with a 2-fold rise in serum TSH, suggesting that leptin acted at hypothalamus in order to stimulate TRH-TSH axis. In addition, BAT D2 was decreased by 25% (p<0.05). In contrast, pituitary D1 showed a 2-fold increase (p<0.001), indicating that, as demonstrated before for liver and thyroid D1, the pituitary enzyme is also acutely up-regulated by leptin. Serum concentrations of insulin and TH of leptin-injected animals remained unchanged. Regulation of 5'-deiodinases directing the local T3 production, is a mechanism by which leptin may alter hypothalamic, pituitary and BAT functions.

Adipose Tissue, Brown↗
PubMed2006

Disruption of neuromedin B receptor gene results in dysregulation of the pituitary-thyroid axis.

The level of thyrotropin (TSH) secretion is determined by the balance of TSH-releasing hormone (TRH) and thyroid hormones. However, neuromedin B (NB), a bombesin-like peptide, highly concentrated in the pituitary, has been postulated to be a tonic inhibitor of TSH secretion. We studied the pituitary-thyroid axis in adult male mice lacking NB receptor (NBR-KO) and their wild-type (WT) littermates. At basal state, NBR-KO mice presented serum TSH slightly higher than WT (18%, P< 0.05), normal intra-pituitary TSH content, and no significant changes in alpha and beta TSH mRNA levels. Serum thyroxine was normal but serum triiodothyronine (T3) was reduced by 24% (P< 0.01) in NBR-KO mice. Pituitaries of NBR-KO mice exhibited no alteration in prolactin mRNA expression but type I and II deiodinase mRNA levels were reduced by 53 and 42% respectively (P< 0.05), while TRH receptor mRNA levels were importantly increased (78%, P< 0.05). The TSH-releasing effect of TRH was significantly higher in NBR-KO than in WT mice (7.1-and 4.0-fold respectively), but, while WT mice presented a 27% increase in serum T3 (P< 0.05) after TRH, NBR-KO mice showed no change in serum T3 after TRH. NBR-KO mice did not respond to exogenous NB, while WT showed a 30% reduction in serum TSH. No compensatory changes in mRNA expression of NB or other bombesin-related peptides and receptors (gastrin-releasing peptide (GRP), GRP-receptor and bombesin receptor subtype-3) were found in the pituitary of NBR-KO mice. Therefore, the data suggest that NB receptor pathways are importantly involved in thyrotroph gene regulation and function, leading to a state where TSH release is facilitated especially in response to TRH, but probably with a less-bioactive TSH. Therefore, the study highlights the important role of NB as a physiological regulator of pituitary-thyroid axis function and gene expression.

Animals↗
PubMed2006

Peptide YY (PYY)3-36 modulates thyrotropin secretion in rats.

Peptide YY (PYY)3-36 is a gut-derived hormone, with a proposed role in central mediation of postprandial satiety signals, as well as in long-term energy balance. In addition, recently, the ability of the hormone to regulate gonadotropin secretion, acting at pituitary and at hypothalamus has been reported. Here, we examined PYY3-36 effects on thyrotropin (TSH) secretion, both in vitro and in vivo. PYY3-36-incubated rat pituitary glands showed a dose-dependent decrease in TSH release, with 44 and 62% reduction at 10(-8) and 10(-6) M (P < 0.05 and P < 0.001 respectively), and no alteration in TSH response to thyrotropin-releasing hormone. In vivo, PYY3-36 i.p. single injection in the doses of 3 or 30 cg/kg body weight, administered to rats fed ad libitum, was not able to change serum TSH after 15 or 30 min. However, in fasted rats, PYY3-36 at both doses elicited a significant rise (approximately twofold increase, P < 0.05) in serum TSH observed 15 min after the hormone injection. PYY3-36 treatment did not modify significantly serum T4, T3, or leptin. Therefore, in the present paper, we have demonstrated that the gut hormone PYY3-36 acts directly on the pituitary gland to inhibit TSH release, and in the fasting situation, in vivo, when serum PYY3-36 is reduced, the activity of thyroid axis is reduced as well. In such a situation, systemically injected PYY3-36 was able to acutely activate the thyrotrope axis, suggesting a new role for PYY3-36 as a regulator of the hypothalamic-pituitary-thyroid axis.

Animals↗
PubMed2005

Prolactin inhibition in lactating rats changes leptin transfer through the milk.

Malnutrition during lactation reduces milk production and changes pup's leptin serum levels. To test prolactin role in this nutritional state, we evaluated whether prolactin suppression during lactation changes serum leptin in dams, its transfer through the milk, and pup's serum leptin. Lactating rats were treated with bromocryptine (1 mg/twice a day, s.c.) or saline three days before sacrifice (days 2-4 or days 19-21). Food intake and body weight were measured until sacrifice (4th and 21st day). Serum prolactin and leptin were determined by radioimmunoassay. Bromocryptine injected dams had lower serum prolactin and milk production as expected. The mothers presented lower food ingestion (day 21: -25%), lower body weight (day 4: -12%; day 21: -10%), higher serum leptin (day 4: +68%), lower milk leptin on the 4th day (11 times) and higher (8 times) on the 21st day. The offspring of bromocryptine-treated mothers presented lower body weight in both periods of lactation and lower serum leptin on the 4th day (-40%) and higher on the 21st day (+37%) of lactation. We suggest that prolactin, through its effect on leptin secretion into the milk, may play an important role in signalizing maternal nutritional status to the pups.

Animals↗
PubMed2003

Increased 5'-iodothyronine deiodinase activity is a maternal adaptive mechanism in response to protein restriction during lactation.

We have shown that protein restriction during lactation is associated with higher levels of serum and milk tri-iodothyronine (T(3)) with lower serum thyroxine (T(4)), suggesting an increased T(4) to T(3) conversion. To investigate this hypothesis, the activity of type 1 (D1) and/or type 2 (D2) iodothyronine deiodinases was evaluated on days 4, 12 and 21 of lactation in several tIssues of dams fed an 8% protein-restricted (PR) diet and controls fed a 23% protein diet. Serum TSH, T(3) and T(4) were measured by radioimmunoassay. Deiodinase activity was determined by the release of (125)I from (125)I-reverse T(3), under specific conditions for D1 or D2. PR dams had a transitory reduction in liver D1 activity (P<0.05) on day 12, and a small increase in thyroid D1 on day 12 followed by a small decrease on day 21. However, thyroid D2 activity was higher than controls (P<0.05) during the whole of the lactation period. Mammary gland D1 and D2 activities were lower on day 4 of lactation in PR dams (P<0.05), and D2 was higher on day 21 (P<0.05). Potentially, a lower conversion of T(3) to di-iodothyronine in the mammary glands of PR dams at the beginning of lactation may serve to provide more T(3) through the milk. Brown adipose tIssue (BAT) D2 activity was higher (P<0.05) in PR dams during all periods of lactation. PR dams showed higher skeletal muscle D1 activity only at the end of lactation, but no changes in D2 activity. Higher pituitary D1 and D2 activities in the PR group (P<0.05) at the end of lactation could have contributed to the lower serum TSH. These data suggest that the higher thyroid and BAT D2 activity during the whole of lactation and skeletal muscle D1 activity at the end of lactation may contribute to the higher serum T(3) in PR dams.

Adaptation, Physiological↗
PubMed2002

The role of leptin in the regulation of TSH secretion in the fed state: in vivo and in vitro studies.

Leptin has been shown to stimulate the hypothalamus-pituitary-thyroid axis in fasting rodents; however, its role in thyroid axis regulation under physiological conditions is still under investigation. Here it was investigated in freely fed rats whether leptin modulates thyrotroph function in vivo and whether leptin has direct pituitary effects on TSH release. Since leptin is produced in the pituitary, the possibility was also investigated that leptin may be a local regulator of TSH release. TSH was measured by specific RIA. Freely fed adult rats 2 h after being injected with a single s.c. injection of 8 microg leptin/100 g body weight showed a 2-fold increase in serum TSH (P<0.05). Hemi-pituitary explants incubated with 10(-9) and 10(-7) M leptin for 2 h showed a reduced TSH release of 40 and 50% respectively (P<0.05). Conversely, incubation of hemi-pituitary explants with antiserum against leptin, aiming to block the action of locally produced leptin, resulted in higher TSH release (45%, P<0.05). In conclusion, also in the fed state, leptin has an acute stimulatory effect on TSH release in vivo, acting probably at the hypothalamus. However, the direct pituitary effect of leptin is inhibitory and data also provide evidence that in the rat pituitary leptin may act as an autocrine/paracrine inhibitor of TSH release.

Animals↗
PubMed2001

Sex steroids modulate rat anterior pituitary and liver iodothyronine deiodinase activities.

In this study, we investigated the sex hormone regulation of 5'-iodothyronine deiodinase activity, which is responsible for enzymatic conversion of thyroxine into the bioactive form, triiodothyronine. Pituitary homogenates and liver microsomes from: 1) ovariectomized rats injected with 17-beta-estradiol benzoate and/or progesterone (0.7 and 250 microg/100 g body weight, respectively, subcutaneously, over 10 days); 2) male castrated rats treated or not with 0.4 mg/100 g body weight testosterone propionate, intramuscular, over 7 days, were assayed for type 1 and type 2 deiodinase activity in the pituitary. Enzyme activities were measured by release of (125)I from deiodination of (125)I reverse triiodothyronine under varying assay conditions. Estrogen stimulated anterior pituitary and liver type 1 deiodinase activity in ovariectomized rats (45 and 30 %, p < 0.05). Progesterone inhibited the liver enzyme (40 %, p < 0.05), and had no effect on the pituitary, but in both tissues, blocked estrogen stimulatory effect on type 1 deiodinase. In males, testosterone normalized the reduced liver type 1 deiodinase of castrated rats. However, in the pituitary, castration increased (50 %) type 1 deiodinase independent of testosterone treatment, suggesting the existence of a inhibitory testicular regulator of pituitary type 1 enzyme. Treatments did not alter pituitary type 2 deiodinase activity. In conclusion, gonads and sex steroids differentially modulate type 1 deiodinase activity in rat pituitary and liver.

Animals↗
PubMed2000

Low-protein diet changes thyroid function in lactating rats.

Lactating rats were fed with free access to an 8% protein-restricted diet (PR); the control group was fed a 23% protein diet (C). An energy-restricted (pair-fed) group was given the same food as the animals in the control group, but the amounts of food consumed by both PF and PR were about the same. The body weight and serum albumin concentration of PR and PF dams were significantly (P < 0. 05) lower than that of the controls. The PR group had a significant increase in serum-free triiodothyronine (FT3) concentration, 24-hr mammary gland and milk radioiodine (I131) uptake (67%, 278%, and 200%, respectively) as compared with the controls. On the other hand, those animals had a significantly lower serum-free thyroxine (FT4) concentration and 2- and 24-hr thyroid I131 uptake (67%, 64%, and 74%, respectively). Protein malnutrition during lactation did not alter thyroid or liver 5'-deiodinase activity significantly. However, PF dams had a significantly lower (25%) thyroid 5'-deiodinase activity. These data suggest that protein-restricted lactating dams had an adaptive change in the thyroid function, which could be important to increase the transference of iodine or triiodothyronine through the milk to their pups and prevent sequelae of neonatal hypothyroidism.

Animals↗
PubMed2000

The somatostatin analogue octreotide modulates Iodothyronine deiodinase activity and pituitary neuromedin B.

Somatostatin inhibits growth hormone and thyrotropin (TSH) secretion. It also enhances the inhibitory effect of thyroid hormone (TH) on TSH by poorly understood mechanisms. We investigated the acute effect of the long-acting somatostatin analogue, octreotide (OCT), on anterior pituitary type 1 (D1) and 2 (D2) deiodinase activity, on liver D1, and on pituitary content of neuromedin B (NB), an autocrine inhibitor of TSH secretion, which is positively regulated by thyroid hormones. Euthyroid or hypothyroid rats were sacrificed at different times after a single subcutaneous injection of OCT (1 microg/kg body weight [BW]). D1 and D2 activities were measured by the release of 125I from 125I reverse triiodothyronine (rT3) under different assay conditions. NB, TSH, T3, and thyroxine (T4) were quantitated by radioimmunoassay (RIA). In euthyroid rats, liver and pituitary D1 activities were decreased (50%) 6 hours after OCT injection; pituitary D2 and NB remained unchanged. In hypothyroid rats, OCT increased near to the level of normal rats both pituitary D1 activity (but not liver) and NB content, at 24 hours and at 6 and 24 hours, respectively (p < 0.05). Pituitary D2, greatly increased by hypothyroidism, showed a small (25%) but significant reduction at 3 hours, persisting at 24 hours (p < 0.01), although it remained higher than that of euthyroid control. Serum thyroid hormones were not affected by OCT injection. The results show that octreotide acutely regulates pituitary deiodinases and NB content, both representing mechanisms that potentially can contribute to somatostatin and octreotide actions on pituitary growth hormone (GH) and TSH secretion and to modulate these cells sensitivity to thyroid hormone action.

Animals↗
PubMed2000

Effect of medroxyprogesterone acetate on thyrotropin secretion in adult and old female rats.

Steroid hormones have been implicated in the modulation of TSH secretion; however, there are few and controversial data regarding the effect of progesterone (Pg) on TSH secretion. Medroxyprogesterone acetate (MPA) is a synthetic alpha-hydroxyprogesterone analog that has been extensively employed in therapeutics for its Pg-like actions, but that also has some glucocorticoid and androgen activity. Both hormones have been shown to interfere with TSH secretion. The objective of the present study was to investigate the effects of MPA or Pg administration to ovariectomized (OVX) rats on in vivo and in vitro TSH release and pituitary TSH content. The treatment of adult OVX rats with MPA (0. 25 mg/100 g body weight, sc, daily for 9 days) induced a significant (P<0.05) increase in the pituitary TSH content, which was not observed when the same treatment was used with a 10 times higher MPA dose or with Pg doses similar to those of MPA. Serum TSH was similar for all groups. MPA administered to OVX rats at the lower dose also had a stimulatory effect on the in vitro basal and TRH-induced TSH release. The in vitro basal and TRH-stimulated TSH release was not significantly affected by Pg treatment. Conversely, MPA had no effect on old OVX rats. However, in these old rats, ovariectomy alone significantly reduced (P<0.05) basal and TRH-stimulated TSH release in vitro, as well as pituitary TSH content. The results suggest that in adult, but not in old OVX rats, MPA but not Pg has a stimulatory effect on TSH stores and on the response to TRH in vitro.

Age Factors↗
PubMed1999

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

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 microM and 10 microM). 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 microM) and 85% (10 microM) 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 microM 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 microg/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.

Analysis of Variance↗
PubMed1998

Effect of testosterone propionate treatment on thyrotropin secretion of young and old rats in vitro.

The aim of this study was to evaluate the influence of androgens on TSH secretion during aging in Dutch rats. Male young (2 months) and old (16-21 months) rats were castrated (Cx) or sham-operated (C) and received testosterone propionate (TP--4 mg/Kg B.W., i.m., 7 days) or vehicle. Female adult (3 months) and old (12 and 17 months) intact rats received TP or corn oil in the same dose. The rats were decapitated, trunk blood was collected and anterior pituitaries were dissected out for in vitro incubation. In Cx young male rats, only TSH pituitary content showed lower levels than in their controls. Cx TP-treated rats showed higher serum TSH and in vitro basal and TRH-induced TSH secretion, but TP only partially reversed the decrease in pituitary TSH promoted by castration. The old male rats showed lower basal in vitro TSH secretion and pituitary TSH content. In Cx old male rats, serum and basal in vitro TSH concentrations were higher than those of old controls and TP treatment further increased basal in vitro TSH secretion, as well as, stimulated TRH-induced TSH secretion. Interestingly, TP had no effect on intact young or old male rats. However, in intact old female rats, TP stimulated in vitro TSH secretion but, as observed in the intact male, TP had no effect on adult female rats. These results suggest a stimulatory role of testosterone on TSH secretion of young and old male rats. Thereafter, it seems that the testes of old rats secrete some testicular factor that inhibits TSH secretion. However, in male rats with normal testosterone levels TP treatment did not increase further TSH secretion, but in old female rats it had a stimulatory effect.

Aging↗
PubMed1998

Nailfold capillaroscopy in hypothyroidism and hyperthyroidism: blood flow velocity during rest and postocclusive reactive hyperemia.

Direct intravital microscopic examinations of nailfold capillaries were made in three groups of subjects: 15 healthy volunteers (C) and 11 patients, six with hypothyroidism (h) and five with hyperthyroidism (H). The groups h and H were examined twice, before the onset of treatment and when they returned to euthyroidism. Capillary blood flow velocity (CBFV) was measured during rest and after release of 60-second arterial occlusion. To assess autoregulatory capacity the authors determined peak CBFV postocclusion and time to reach it in single capillaries. In patients with hypothyroidism, before the onset of the treatment, the mean resting and the mean peak CBFV were significantly lower (resting CBFV-group C: 0.93+/-0.11 mm/s (mean+/-SE); group h: 0.33+/-0.09 mm/s; and mean peak CBFV-group C: 1.49+/-0.14 mm/s; group h: 0.79+/-0.19 mm/s). The time to reach mean peak CBFV postocclusion was significantly prolonged (group C: 8.9+/-0.65 s and group h: 19.2+/-2.0 s) compared with the group of healthy volunteers. When these patients achieved euthyroidism, all the studied parameters returned to control levels. In patients with hyperthyroidism only minor changes in CBFV could be detected. In patients with hypothyroidism, the skin microvascular autoregulatory mechanisms are disturbed. The impairments of the reactive hyperemia response could be correlated with the control of the disease (thyroid state).

Adult↗
PubMed1997

Pituitary neuromedin B content in experimental fasting and diabetes mellitus and correlation with thyrotropin secretion.

Fasting and diabetes mellitus in the rat model have been associated with abnormalities of thyrotropin (TSH) secretion. Neuromedin B is a bombesin-like peptide highly concentrated in the pituitary gland that has been shown to have inhibitory action on TSH secretion, acting as an autocrine/paracrine factor. Here, we aimed to determine if the pituitary content of neuromedin B would change in fasted rats (1, 2, 3, and 4 days of food deprivation) and streptozotocin (55 mg/kg body weight)-diabetic rats. The total pituitary content of neuromedin B was decreased in fasted rats, except at 2 days of fasting, as was the total protein content in the gland; however, the concentration of the peptide (femtomoles per milligram protein) did not significantly change until the fourth day of food deprivation, when an abrupt decrease in total protein happened and therefore neuromedin B concentration increased. In rats after 20 days of diabetes induction, pituitary neuromedin B increased. Serum thyroxine (T4) and triiodothyronine (T3) decreased in both disorders, whereas serum TSH was normal or decreased in 4-day fasted rats. Therefore, the caloric deprivation of diabetes and fasting changed the pituitary neuromedin B content and concentration, by mechanisms that remain to be elucidated. Since neuromedin B has been shown to act as a local inhibitor of TSH release, the results raise the possibility that increased neuromedin B concentration might be involved in the altered TSH secretion of diabetes mellitus and fasting.

Animals↗
PubMed1997

Dose-dependent effects of 17-beta-estradiol on pituitary thyrotropin content and secretion in vitro.

We studied the basal and thyrotropin-releasing hormone (TRH) (50 nM) induced thyrotropin (TSH) release in isolated hemipituitaries of ovariectomized rats treated with near-physiological or high doses of 17-beta-estradiol benzoate (EB; sc, daily for 10 days) or with vehicle (untreated control rats, OVX). One group was sham-operated (normal control). The anterior pituitary glands were incubated in Krebs-Ringer bicarbonate medium, pH 7.4, at 37 degrees C in an atmosphere of 95% O2/5% CO2. Medium and pituitary TSH was measured by specific RIA (NIDDK-RP-3). Ovariectomy induced a decrease (P < 0.05) in basal TSH release (normal control = 44.1 +/- 7.2; OVX = 14.7 +/- 3.0 ng/ml) and tended to reduce TRH-stimulated TSH release (normal control = 33.0 +/- 8.1; OVX = 16.6 +/- 2.4 ng/ml). The lowest dose of EB (0.7 microgram/100 g body weight) did not reverse this alteration, but markedly increased the pituitary TSH content (0.6 +/- 0.06 microgram/hemipituitary; P < 0.05) above that of OVX (0.4 +/- 0.03 microgram/hemipituitary) and normal rats (0.46 +/- 0.03 microgram/hemipituitary). The intermediate EB dose (1.4 micrograms/100 g body weight) induced a nonsignificant tendency to a higher TSH response to TRH compared to OVX and a lower response compared to normal rats. Conversely, in the rats treated with the highest dose (14 micrograms/100 g body weight), serum 17-beta-estradiol was 17 times higher than normal, and the basal and TRH-stimulated TSH release, as well as the pituitary TSH content, was significantly (P < 0.05) reduced compared to normal rats and tended to be even lower than the values observed for the vehicle-treated OVX group, suggesting an inhibitory effect of hyperestrogenism. In conclusion, while reinforcing the concept of a positive physiological regulatory role of estradiol on the TSH response to TRH and on the pituitary stores of the hormone, the present results suggest an inhibitory effect of high levels of estrogen on these responses.

Animals↗
PubMed1997

Effects of estradiol benzoate on 5'-iodothyronine deiodinase activities in female rat anterior pituitary gland, liver and thyroid gland.

There is little information on the possible effects of estrogen on the activity of 5'-deiodinase (5'-ID), an enzyme responsible for the generation of T3, the biologically active thyroid hormone. In the present study, anterior pituitary sonicates or hepatic and thyroid microsomes from ovariectomized (OVX) rats treated or not with estradiol benzoate (EB, 0.7 or 14 micrograms/100 g body weight, s.c., for 10 days) were assayed for type I 5'-ID (5'-ID-I) and type II 5'-ID (5'-ID-II, only in pituitary) activities. The 5'-ID activity was evaluated by the release of 125I from deiodinated 125I rT3, using specific assay conditions for type I or type II. Serum TSH and free T3 and free T4 were measured by radioimmunoassay. OVX alone induced a reduction in pituitary 5'-ID-I (control = 723.7 +/- 67.9 vs OVX = 413.9 +/- 26.9; P < 0.05), while the EB-treated OVX group showed activity similar to that of the normal group. Thyroid 5'-ID-I showed the same pattern of changes, but these changes were not statistically significant. Pituitary and hepatic 5'-ID-II did not show major alterations. The treatment with the higher EB dose (14 micrograms), contrary to the results obtained with the lower dose, had no effect on the reduced pituitary 5'-ID-I of OVX rats. However, it induced an important increment of 5'-ID-I in the thyroid gland (0.8 times higher than that of the normal group: control = 131.9 +/- 23.7 vs OVX + EB 14 micrograms = 248.0 +/- 31.2; P < 0.05), which is associated with increased serum TSH (0.6-fold vs OVX, P < 0.05) but normal serum free T3 and free T4. The data suggest that estrogen is a physiological stimulator of anterior pituitary 5'-ID-I and a potent stimulator of the thyroid enzyme when employed at high doses.

Analysis of Variance↗
PubMed1996

Effect of thyroid hormones on pituitary neuromedin B and possible interaction between thyroid hormones and neuromedin B on thyrotropin secretion.

Neuromedin B (NB), a bombesin-like peptide, has been recently characterized as a physiological paracrine/autocrine inhibitor of thyrotropin (TSH) secretion. We hypothesized on the basis of our prior experiments that thyroid hormones stimulate pituitary NB secretion which mediates, at least in part, the TSH-suppressive effect of thyroid hormone. Here, we evaluated the time-course of the effect of thyroid hormones administration to eu- and hypothyroid rats on the anterior pituitary content of NB and on serum TSH. As previously reported, the pituitary content of NB increased in hyperthyroidism and decreased in hypothyroidism. Chronic treatment of hypothyroid rats with a physiological dose of thyroxine (0.8 microgram/100 g b.w. s.c, for 3 or 5 days) normalized pituitary NB content, while 5 days of treatment with a pharmacological dose of thriiodothyronine (0.4 microgram/100 g b.w.) induced an increase above that of normal pituitaries. Thyroxine and triiodothyronine injected once, s.c., into hypothyroid rats required 30 min to normalize NB content, which reached higher than normal values in 3-6 h. At these times, the increment in NB preceded or was simultaneous with the suppression of serum TSH. This rapid and marked effect on pituitary neuromedin B content, associated in time with TSH suppression, is in agreement with the hypothesis that neuromedin B may mediate at least in part, the acute suppression of TSH release by thyroid hormone, a hypothesis that still needs further verification.

Animals↗