The effects of sex steroids on thyroid C cells and trabecular bone structure in the rat model of male osteoporosis

Androgen deficiency is one of the major factors leading to the development of osteoporosis in men. Since calcitonin (CT) is a potent antiresorptive agent, in the present study we investigated the effects of androgen deficiency and subsequent testosterone and estradiol treatment on CT-producing thyroid C cells, skeletal and hormonal changes in middle-aged orchidectomized (Orx) rats. Fifteen-month-old male Wistar rats were either Orx or sham-operated (SO). One group of Orx rats received 5 mg kg⁻¹ b.w. testosterone propionate (TP) subcutaneously, while another group was injected with 0.06 mg kg⁻¹ b.w. estradiol dipropionate (EDP) once a day for 3 weeks. A peroxidase–antiperoxidase method was applied for localization of CT in the C cells. The studies included ultrastructural microscopic observation of these cells. The metaphyseal region of the proximal tibia was measured histomorphometrically using an imagej public domain image processing program. TP or EDP treatment significantly increased C cell volume (Vc), volume densities (Vv) and serum CT concentration compared with the Orx animals. Administration of both TP and EDP significantly enhanced cancellous bone area (B.Ar), trabecular thickness (Tb.Th) and trabecular number (Tb.N) and reduced trabecular separation (Tb.Sp). Serum osteocalcin (OC) and urinary Ca concentrations were significantly lower after these treatments in comparison with Orx rats. These data suggest that testosterone and estradiol treatment in Orx middle-aged rats affect calcitonin-producing thyroid C cells, which may contribute to the bone protective effects of sex hormones in the rat model of male osteoporosis.     

Cellular proliferation in the anterior pituitary gland of normal adult rats: Influences of sex,estrous cycle,and circadian change

Proliferative activity of the anterior pituitary gland in 10 week-old male and female rats under normal conditions was investigated by counting mitotic figures and using single and double immunostaining of 5-bromo-2′-deoxyuridine (BrdU), proliferating cell nuclear antigen (PCNA), and six pituitary hormones. To determine which proliferative changes depend on the estrous cycle and circadian changes, respectively, six groups of female and two groups of male rats were studied at various times of day. Additionally, BrdU-incorporated cells were further classified by the six types of hormones they contained, or as immunonegative cells. Cell proliferative activity in the females fluctuated drastically with the highest activity in estrus and the lowest in diestrus. In the males, proliferative activity was at a relatively low level, and was similar to that in females in proestrus or early estrus, with the greater activity at night. Identified by their pituitary hormones, the distribution of the proliferating cells was almost the same in each sex, with prolactin (PRL) cells accounting for the highest proportion, followed by growth hormone (GH) cells, and adrenocorticotropic hormone (ACTH), luteinizing hormone (LH), follicle stimulating hormone (FSH), and thyroid stimulating hormone (TSH) cells. These percentages agreed well with previously reported levels of cell types among all pituitary cells of the rat. It is therefore suggested that the life span and cycle of rat pituitary cells does not differ among cell types. In another test, male and female rats were given BrdU continuously via an osmotic pump for 8 days to compare cell proliferative activity between sexes, exclusive of the influence of estrous cycle and circadian changes. In this way, we were able to demonstrate that the cumulative incorporation of BrdU in females was consistently twice as high as in males over a constant period of time, and to conclude that cell renewal occurs at a doubled rate in the pituitary of female rat. © Wiley-Lis, Inc.     

The ultrastructure of the thyrotropic cell during thyrotropin rebound in the adenohypophysis of the rat

Adenohypophyses of rats were studied ultrastructurally to ascertain the morphologic changes that occur in thyrotropic cells during the pituitary TSH Rebound Phenomenon. Rats were maintained on propylthiouracil (PTU) for 43–147 days and their adenohypophyses studied three to nine days after discontinuance of goitrogen treatment. TSH rebound was also induced in chronically hypothyroid rats by single intravenous injections of 0.8, 4, 20 and 200 μg of thyroxine. Pituitaries were studied from animals sacrificed 6–24 hours after thyroxine injection. Thyrotrophs of euthyroid rats were characterized ultrastructurally by the presence of numerous peripherally-located, small secretory granules (storage phase) and by highly dilated cisternae of rough endoplasmic reticulum (secretory phase). The thyrotropic cells in PTU-treated rats were sparsely granulated, displayed enlarged mitochondria with much loss of cristae and contained extensively dilated rough endoplasmic reticulum and expanded Golgi membranes. Marked repletion of granules, both intracisternal and cytoplasmic, was seen during TSH rebound in the pituitary. It was observed in some thyrotrophs as early as three days after goitrogen withdrawal and was enhanced further at the 6- and 9-day intervals. Granule repletion increased progressively with doses of thyroxine up to 20 μg and assayable thyrotropin in pituitary glands increased 500–700% over normal. Effects with the 20 μg dose could be detected as early as six hours. With higher doses of thyroxine, granule repletion in thyrotrophs was inhibited and mitcohondrial hypertrophy was largely reversed. The electron microscopic findings reveal close correlation with previously published data on thyrotropin assays of the rat pituitary. They support the concept that the degree of cytoplasmic granulation in thyrotropic cells is quantitatively related to assayable stores of thyrotropin in the anterior pituitary gland.     

Morphologic effects of bromocriptine on spontaneously occurring pituitary prolactin-cell hyperplasia in old Long-Evans rats.

The effect of bromocriptine (BEC), a dopaminergic agonist, on nontumorous pituitary prolactin (PRL) cells of aging female Long-Evans rats, was studied histologically, immunocytologically, electron-microscopically, and morphometrically. Rats were arbitrarily divided into two control groups, one with normal (less than 20 ng/ml) and one with elevated serum PRL concentrations, and into four BEC-treated groups, all of which had increased serum PRL levels prior to commencement of BEC administration. In hyperprolactinemic control rats, compared with normoprolactinemic control rats, pituitary weight and percentage of pituitary PRL cells were increased. The morphologic features of PRL cells in these two groups did not differ markedly, which suggested that hyperprolactinemia was due to increased PRL-cell number and not increased PRL-cell function. Compared with age-matched hyperprolactinemic control rats, hyperprolactinemic rats treated with BEC showed a reversible decrease in serum PRL levels, pituitary weight as well as percentage of pituitary PRL cells, and by ultrastructural morphometry an increase in the volume density of lysosomes. BEC caused no striking changes in nuclear and cytoplasmic areas, volume densities of RER, Golgi regions, mitochondria, lipid droplets, and size and volume densities of forming and storage granules. Since spontaneously hyperplastic PRL cells show less conspicuous morphologic changes following BEC treatment than PRL cells rendered hyperplastic by estrogen administration or pituitary transplantation, it is suggested that PRL cells with no increased endocrine function respond less markedly to dopaminergic suppression than endocrinologically hyperactive PRL cells. It can be concluded that BEC suppresses spontaneous proliferation of PRL cells which occurs with aging.     

Free alpha subunit of the pituitary glycoprotein hormones. Measurement in serum and tissue of patients with pituitary tumors.

A solid-phase radioimmunoassay was developed that measures the free alpha subunits of pituitary glycoprotein hormones (alpha PGpHs) and has negligible cross-reactivity with the intact hormones (less than 0.014% for thyroid-stimulating hormone [TSH], less than 0.1% for human chorionic gonadotropin [hCG], 0.8% for luteinizing hormone [LH], and 2.0% for follicle-stimulating hormone [FSH]). The assay is standardized with the alpha subunit of hCG but also reacts well with the alpha subunits of the other glycoprotein hormones (84% for alpha TSH, 77% for alpha FSH, and 64% for alpha LH). Concentrations as low as 0.3 micrograms/L can be reliably measured, and the 97.5% reference range in 27 healthy adults, including postmenopausal females, is less than or equal to 1.2 micrograms/L. Elevated preoperative alpha PGpH concentrations were found in 45 (9.4%) of 479 sera from patients with pituitary adenoma and 3 (4.5%) of 66 patients with nonadenomatous sellar lesions. Postoperative alpha PGpH levels were lower in 30 of 39 adenoma patients and 2 of 3 nonadenoma patients. In five (1%) of the patients with pituitary adenomas, alpha PGpH was the only elevated serum hormone marker. Serum values of alpha PGpH correlate weakly with alpha subunit immunocytochemical staining--95% of those with negative staining have normal alpha PGpH values, but only 18% of those with positive staining have elevated alpha PGpH values.     

Changes in pituitary and thyroid function with increasing age in young male rats.

As the age of young adult male rats increased from 30 to 150 days, the serum thyroxine (T4) decreased by 50% and the serum thyroid-stimulating hormone (TSH) increased by 250%. There was no change in the serum triiodothyronine (T3). The increment in serum TSH after injection of thyrotropin-releasing hormone (TRH) was not significantly different at any of the ages studied, but the old animals had significantly lower increments in serum T4 and T3 after subcutaneous administration of bovine TSH. Despite a higher basal serum TSH, the older rats had a lesser increase in serum TSH after thyroidectomy or propylthiouracil. Thus, 1) there is a progressive decline in intrinsic thyroid function between 30 and 150 days of age in male rats, and 2) pituitary TSH response to fall in serum concentration of thyroid hormones is also decreased with age.     

Effect of Prolactin on the Population of Epithelial Cells From Ventral Prostate of Intact and Cyproterone Acetate‐Treated Peripubertal Rats: Stereological and Immunohistochemical Study

The interactions between steroid and nonsteroid hormones in the prostate are of special interest during the growth phase of the gland. The purpose of this work is to study the influence of prolactin (PL), with or without androgenic blockade, on epithelial cells from peripubertal rat ventral prostate. Twenty male peripubertal Sprague‐Dawley rats were grouped as controls, or treated with cyproterone acetate (CA), CA plus PL (CA‐PL), or PL. The total number (N total) of epithelial cells, and their labeling indices to proliferative cell nuclear antigen (LI PCNA), apoptosis (LI apoptosis) and androgen receptors (LI AR) were measured. CA and PL treatment significantly decrease the N total, but the LI PCNA was unchanged. We have observed a greater LI apoptosis in pharmacologically castrated animals without PL than in the rats with androgenic blockade with PL. The LI AR does not change with CA treatment in the ventral region, but the PL significantly increases it. Androgenic blockade and PL decrease the number of epithelial cells from the ventral prostate. These changes are not attributable to the decrease of cell proliferation, rather to the increase of epithelial apoptosis. The increase of cells expressing AR after treatment with PL might be attributed to the decrease of testosterone secretion caused by the hyperprolactinemia. PL does not modulate the size of the ventral prostate in prepubertal rats. Anat Rec, 2009. © 2009 Wiley‐Liss, Inc.     

In vitro TSH and PRL secretion from eutopic and heterotopic rat pituitaries: effects of hypothyroidism

Five adenohypophyses from donors of the same strain, age, and sex were transplanted under the renal capsule of young adult female rats. At least 3 wk later, enzymatically dispersed cells from eutopic or heterotopic adenohypophyses from the same rat were perifused in vitro in a small chamber. Thyrotropin (TSH) and prolactin (PRL) secretion per 10(6) cells were significantly less from heterotopic than from eutopic cells under all conditions. In cells from euthyroid animals, TRH induced TSH secretion only in the eutopic cells but induced PRL secretion in both eutopic and heterotopic cells. Hypothyroidism increased TRH-induced TSH secretion and content in the cell lysate in both eutopic and heterotopic cells but increased TRH-induced PRL secretion only in the eutopic cells. The increase in TSH secretion induced by hypothyroidism in the heterotopic cells was of borderline statistical significance. The inability of TRH to induce TSH secretion in heterotopic pituitary cells from euthyroid rats may be due to a lower set point for thyroid hormone inhibition of TSH secretion in the heterotopic thyrotrophs. Heterotopic pituitary TSH secretion is probably suppressed by the normal plasma thyroid hormone concentration maintained by the eutopic pituitary and may be stimulated by TRH only in the presence of a subnormal plasma thyroid hormone concentration.     

Daily rat tibial growth in vivo following hypothalamic sex reversal with neonatal and pubertal treatments with gonadal steroids

Summary. A striking sex-related difference in postpubertal growth and growth hormone (GH) secretory pattern in the rat has been described. Although this sexual dimorphism seems to be determined by the neonatal effects of gonadal steroids on the hypothalamus, peripubertal exposure to steroids also plays an important role. In order to study the real influence of the hypothalamic sex and/or peripubertal gonadal steroids, the growth pattern of female and male rats in response to neonatal and peripubertal sexual steroid treatments was studied using microknemometry, a technique that allows non-invasive daily measurements of rat tibial growth rate. Neonatal steroid environment in males was modified by castration on day 1, whereas in females it was changed by a single neonatal testosterone administration on day 5 followed by castration at 13 days of age. From the onset of puberty to adulthood, both female and male animals received testosterone or estrogens, respectively. Neonatal treatment alone, i.e. androgenization of female and castration of male rats, were only able to induce a partial reversal of the original sex-dependent growth pattern. Additional peripubertal treatments achieved a complete change in the sex-linked growth pattern. Consistent with the effects observed on growth, the pituitary GH concentration was significantly increased in females, and diminished in males, when they were treated both at the neonatal and peripubertal stages. However, only this latter group, whose growth was more seriously compromised, showed decreased plasma insulin-like growth factor-I (IGF-I) levels. In conclusion, a complete feminization of male tibial growth pattern or masculinization of female pattern can only be achieved by maintaining the new steroid environment from puberty to adulthood.     

Daily rat tibial growth in vivo following hypothalamic sex reversal with neonatal and pubertal treatments with gonadal steroids

A striking sex-related difference in postpubertal growth and growth hormone (GH) secretory pattern in the rat has been described. Although this sexual dimorphism seems to be determined by the neonatal effects of gonadal steroids on the hypothalamus, peripubertal exposure to steroids also plays an important role. In order to study the real influence of the hypothalamic sex and/or peripubertal gonadal steroids, the growth pattern of female and male rats in response to neonatal and peripubertal sexual steroid treatments was studied using microknemometry, a technique that allows non-invasive daily measurements of rat tibial growth rate. Neonatal steroid environment in males was modified by castration on day 1, whereas in females it was changed by a single neonatal testosterone administration on day 5 followed by castration at 13 days of age. From the onset of puberty to adulthood, both female and male animals received testosterone or estrogens, respectively. Neonatal treatment alone, i.e. androgenization of female and castration of male rats, were only able to induce a partial reversal of the original sex-dependent growth pattern. Additional peripubertal treatments achieved a complete change in the sex-linked growth pattern. Consistent with the effects observed on growth, the pituitary GH concentration was significantly increased in females, and diminished in males, when they were treated both at the neonatal and peripubertal stages. However, only this latter group, whose growth was more seriously compromised, showed decreased plasma insulin-like growth factor-I (IGF-I) levels. In conclusion, a complete feminization of male tibial growth pattern or masculinization of female pattern can only be achieved by maintaining the new steroid environment from puberty to adulthood.     

Methimazole interferes with the progression of experimental autoimmune myocarditis in rats

We produced experimental autoimmune hypophysitis (EAH) in rats and investigated its characteristics. Female Lewis rats were immunized by two injections with homologous pituitary homogenate and complete Freund's adjuvant. Blood was collected serially from the rats, and serum antibodies to pituitary antigens were examined. The rats were sacrificed 2 or 4 weeks after the final immunization, and histological examinations of the endocrine organs were carried out. Histological examination revealed slight, focal infiltration of mononuclear cells in the pituitary gland only in the rats immunized with the pituitary homogenate. Infiltration of mononuclear cells was not observed in the thyroid gland, pancreas, adrenal gland, or ovary. In the serological examination, antibodies to both cytosolic antigens and cytoplasmic particle antigens from the pituitary gland were detected by enzyme-linked immunosorbent assay (ELISA), and these antibody levels increased with time. Western blotting using the serum antibodies identified an immunoreactive protein of approximately 21.5 kDa among these antigens, and we confirmed that this protein was rat growth hormone (GH). Furthermore, antibodies to GH, thyrotropin (TSH), and luteinizing hormone (LH) were detected by ELISA. Antibodies to follicule stimulating hormone, prolactin, or adrenocorticotropin were not detected. These data suggest that several antigens from the pituitary gland are involved in EAH in rats, and that GH, TSH, and LH are major antigens among the pituitary antigens in this model.     

Binding of bovine and porcine pituitary glycoprotein hormone alpha-subunit to TSH antibody in serum of patients with Graves' disease.

The characteristics of autoantibodies reactive with bovine (b) TSH were examined in the sera of six patients with Graves' disease selected on the basis of highly negative values in the TSH receptor assay. Test sera were incubated with other 125I-labeled pituitary glycoprotein hormones and their isolated subunits (alpha and beta) [human (h) TSH, bTSH, porcine (p) TSH, pFSH, bFSH, bLH and equine (e) chorionic gonadotropin (CG)] (purity was confirmed by gel-filtration on Sephadex G-100 and SDS-PAGE), and the antibody bound fraction was precipitated by the addition of anti-human gamma-globulin (goat). Almost all sera showed detectable binding to bTSH, pTSH, pFSH, pTSH-alpha, bFSH-alpha, bLH-alpha, but not to hTSH, hTSH-alpha, hTSH-beta, hFSH, hLH, hCG, pTSH-beta, bLH-beta, eCG-alpha. Exceptions were very low binding to bLH-beta by one serum and to pTSH-beta, by two sera. The level of binding (B/T%) of the patients' sera to pTSH-alpha, bFSH-alpha and bLH-alpha was 3.0-27.7%, 2.6-45.3% and 2.2-39.0%, respectively; that of sera from normal healthy adults was 1.9 +/- 0.3%, 0.8 +/- 0.2% and 0.9 +/- 0.2% (mean +/- SD), respectively. These results indicate that the TSH antibodies recognize mainly an epitope in the alpha subunit of bovine and porcine pituitary glycoprotein hormones (TSH, FSH, LH).     

Characterization of monoclonal antibodies against human thyrotropin and use in an immunoradiometric assay and immunohistochemistry

Monoclonal antibodies were prepared against human thyrotropin. 13 different antibodies were characterized. Ten antibodies were of the IgG1 subclass. The affinities of the antibodies were in the range 10(9)-10(11) mol-1 X l. Four of them were specific for hTSH and did not react with hLH, hFSH, hCG or alpha hCG. Four reacted with these hormones and recognized the alpha subunit of hCG. One cross-reacted only with hFSH. The remaining four antibodies recognized the holo-hTSH only, and thus were designated as anti-conformational determinants. Monoclonal antibodies reacting with different antigenic determinants on the hTSH molecule defined seven clusters. Two of them were used to develop a simplified two-site sandwich radioimmunoassay in which one monoclonal antibody was immobilized on tubes (anti-beta TSH) and another (anti-alpha) labelled with 125I. This assay was highly specific and demonstrated a sensitivity level of 0.1 microIU/ml. Two monoclonal antibodies were used in immunohistochemistry and their quality and specificity was assessed in the detection of hTSH immunoreactivity in human pituitary biological sections.     

Immunocytochemical hormonal features of pituitary adenomas of aging Wistar male rats

Pituitary adenomas were the most common grossly visible naturally occurring neoplasms found in over 27% of rats surviving beyond 17 months of age. Twenty-three pituitary adenomas, fixed in buffered neutral formalin and embedded in paraffin, were tested for the presence of prolactin (PRL), growth hormone (GH) and thyroid stimulating hormone (TSH) using the unlabeled peroxidase-antiperoxidase method. The adenoma cells in 6 (26%) of the 23 tumors stained with two or three of the tested hormones, but clear evidence that individual neoplastic cells contained more than one hormone was not found. These findings suggest that in aging male Wistar rats the spontaneous pituitary adenomas may originate from undifferentiated cells, PRL-, GH- and TSH-cells in a diminishing order of frequency.     

Pituitary nuclear triiodothyronine receptors during development in the rat

Studies were undertaken to measure the pituitary nuclear triiodothyronine (T3) binding capacity (BC) during development in the rat. BC was measured in 0.4 M NaCl-solubilized receptors in 5-, 14-, 20-, 27-, 30-, 40-, 50-day-old rats and in adult animals. Results indicate that BC is lower in 5-day-old rats than in adult animals (0.397 +/- 0.02 vs. 0.797 +/- 0.06 pmol T3/mg protein) (mean +/- SE) (P less than 0.01). Hypothyroidism, induced during the neonatal period or in the adult animal, results in a significant decrease in BC (P less than 0.01) when compared with control rats. However, treatment of hypothyroid animals with T3 (0.4 micrograms/100 g body wt) for a period of 7-14 days significantly increased BC as compared with hypothyroid rats without apparent changes in Ka. The relative affinities of various thyroid hormone analogues for the nuclear receptor were also measured in the adult animal. The affinities of these analogues are in the following order: TRIAC greater than L-T3 greater than D-T3 greater than L-T4 greater than D-T4 greater than DIMIT greater than L-T2 greater than rT3. The present findings demonstrate the presence of high affinity nuclear T3 binding sites in the pituitary of neonatal rat and could thus account for the effects of thyroid hormones on GH synthesis and TSH secretion observed in these animals.     

hCG对葡萄胎患者甲状腺机能的影响

应用放射免疫和免疫放射方法测定１３例葡萄胎患者的ｈＣＧ水平及甲状腺功能。结果：Ｔ４、ＦＴ４水平升高，Ｔ３浓度较正常为高（Ｐ〈０．００１），少数病例ＦＴ３水平升高。葡萄胎组织清除后，Ｔ４、ＦＴ４、Ｔ３随ｈＣＧ水平下降而下降，ｈＣＧ浓度与三者之间成正相关关系。ｈＣＧ浓度与ＴＳＨ水平呈现镜像（ｍｉｒｒｏｒ ｉｍａｇｅ）关系。结果提示：在葡萄胎患者，其甲状腺功能亢进并非由垂体分泌的ＴＳＨ刺激所致，而是受到     

Monoclonal Antibodies Against Human Chorionic Gonadotropin (hCG): I. Production,Specificity, and Intramolecular Binding Sites*

ABSTRACT: Thirty-nine monoclonal antibody (MCA) producing hybridoma cell lines derived from fusions of mouse myeloma cells with spleen cells from mice immunized with human chorionic gonadotropin (hCG) have been established. Their products have been tested in radioimmunoassays using ¹²⁵I-labeled hCG, luteinizing hormone (LH), follicle-stimulating hormone (FSH), thyroid-stimulating hormone (TSH), the alpha (α) and beta (β) subunits of hCG and LH, and the C-terminal peptide 109–145 (CTP) of CG. All MCA were, in addition, tested in indirect immunofluorescence (IIF) on paraffin sections of human pituitary glands. According to the intramolecular localization of the determinants recognized, three main groups of MCA can be distinguished: 1) MCA directed against epitopes on the β-chain (α-MCA), 2) MCA directed against (β-chain determinants (β-MCA), and 3) MCA reacting with a conformational determinant only present on the native hormone and not on either subunit (con-formational-MCA). All α-MCA cross-react with human LH, FSH, and TSH. The β-MCA do not react with FSH or TSH, but do react to a varying degree with LH. The conformational-MCA show no binding of labeled FSH or TSH and very little or no cross-reactivity with LH.     

DNA diagnosis in endocrinological disease--pituitary disease]

Endocrine disorders have long been diagnosed by symptoms, before hormones were able to be measured by immunoassays. Recently, as molecular biological methods developed, DNA diagnosis has become available in many diseases including endocrine disorders. We present here DNA diagnosis in connection with anterior pituitary hormones. Our studies on thyrotropin (TSH) producing pituitary adenomas showed that TSH beta-subunit mRNAs of the adenomas were the same as those from normal pituitary tissues. Congenital isolated TSH deficiency is rare disease causing hypothyroidism including cretinism, severe mental and growth retardation. We have studied 3 families with consanguineous marriage and 2 families which were descendants of closed colonies. The molecular pathogenesis were elucidated in the cases of 3 Japanese families with consanguineous marriage. They had a same missense mutation in the 2nd exon of the TSH beta-subunit gene which made a restriction enzyme site, and could be analyzed either by genomic Southern blot analyses or by restriction enzyme digestion after amplification of genomic DNA by PCR. Congenital deficiency of growth hormone, prolactin, and TSH was first described in Snell dwarf mice. The gene encoding the nuclear factor Pit-1/GHF-1, which transactivates promoters of both growth hormone gene and prolactin gene, was shown to be the cause of Snell dwarf mice. A similar human case arose from a family with consanguineous marriage, and the relation with the pit-1/GHF-1 gene is now under study.     

Effect of diphenylhydantoin on hypothalamic-pituitary-thyroid function in the rat

Chronic diphenylhydantoin (DPH) administration (5 mg x 100 g body wt-1 x day-1) to the normal rat is associated with a decrease in the serum thyroxine (T4) and triiodothyronine (T3) concentrations without an appropriate rise in the serum thyrotropin (TSH) concentration, suggesting a possible direct effect of DPH on TSH secretion. To further study this possibility, DPH was administered chronically to thyroidectomized, hypothyroid rats. In the hypothyroid rats treated chronically with DPH, serum TSH did not increase, pituitary TSH content was significantly decreased, and the serum TSH response to thyrotropin-releasing hormone (TRH) was decreased compared to that of diluent-treated, hypothyroid rats. Hypothalamic TRH content was similar in DPH and diluent-treated rats. These findings suggest that DPH suppresses pituitary TSH secretion, probably as a thyroid hormone agonist. The effect of a single large dose of DPH (20 mg/100 g body wt) administered to thyroidectomized rats also decreased serum tSH but, in contrast to the findings in chronically treated rats, hypothalamic TRH and pituitary TSH content and the serum TSH responses to TRH were increased. These differences may be due to the acute inhibitory effect of a large dose of DPH on hypothalamic TRH release. Furthermore, because the effect of thyroid hormone on regulating pituitary TSH synthesis and release is dose and time dependent, the effect of DPH as a thyroid hormone agonist on pituitary TSH dynamics may also be variable.     

人绒毛膜促性腺激素对早孕妇女甲状腺机能的影响

本文应用放射免疫（ＲＩＡ）和免疫放射（ＩＲＭＡ）方法对２０例早孕妇女的人绒毛膜促性腺激素（ｈＣＧ）水平进行研究，以求阐明是否ｈＣＧ具有垂体促甲状腺激素（ＴＳＨ）样作用的可能性。结果显示，甲孕妇女四碘甲状腺原氨酸（Ｔ４）和游离甲状腺素（ＦＴ４）水平升高，ｈＣＧ浓度与Ｔ４、ＦＴ４亦成正相关关系，然其三碘甲状腺原氨酸（Ｔ３）、游离三碘甲状腺原氨酸（ＦＴ３）水平却与正常对照组无明显差异。ｈＣＧ水平升高与Ｔ