(1/770) Effect of hypophysectomy on hypothalamic somatostatin content in rats.
The effect of hypophysectomy on the hypothalamic somatostatin content was examined in rats. Somatostatin content in the acid extract of the pituitary stalk and the median eminence tissue (SME) was measured by specific radioimmunoassay. In young male rats, the mean somatostatin content in SME was 63.9+/-5.0 ng. Two weeks after hypophysectomy, it was reduced significantly to 34.4+/-3.3 ng. The result may indicate that the elimination of feedback actions of GH and/or TSH on the hypothalamus led to the decreased synthesis and/or the release of somatostatin. However, the possibility that structural changes in the pituitary stalk and the median eminence tissue ensued after hypophysectomy resulted in the depletion of somatostatin cannot be ruled out. (+info)
(2/770) Inhibitory effect of plasma obtained from hypophysectomized and control women on the assay of bioactive luteinizing hormone.
The purpose of this study was to determine the effect of components of female plasma on the value of bioactive luteinizing hormone (LH), especially in the presence of low immunological LH value. Using both an immunoradiometric assay (IRMA) and rat Leydig cell bioassay, immunoreactive (I) and bioactive (B) LH were assessed in plasma collected from women during a gonadotrophin releasing hormone (GnRH) test performed on day 7 of a spontaneous cycle. Two modes of response to an acute administration of GnRH were defined: normal production of gonadotrophins (group I) and excessive secretion (group II) associated with a significant difference in the B/I-LH ratio between the two groups. The B/I-LH ratio did not vary with sampling time during the test in either group. The addition of LH-free plasma collected from hypophysectomized women caused a 30% decrease in testosterone production compared to control values (in the presence or absence of hLH standard). A partial restoration of testosterone production was observed if plasma was first treated with PEG 12%. The inhibitory factor(s) was also present in plasma from ovulatory women, even after treatment by an antibody against the entire LH molecule. The effect of normal (A) or low I-LH plasma (B) on testosterone production varied strongly according to the plasma volume added to the bioassay, as well as to plasma treatments. Diethylether treatment caused a 50% decrease in testosterone secretion for plasma B (but not for A) whereas a diminution of the steroidogenesis is observed after a PEG treatment of plasma A (but not for B), suggesting that different inhibitory factors are present in plasmas A and B. Therefore the LH bioactivity measured in the rat Leydig cell assay, in terms of testosterone output, seems to represent a balance between the LH molecule and the presence of inhibitory factors in the plasma. (+info)
(3/770) Is the primitive regulation of pituitary prolactin (tPRL177 and tPRL188) secretion and gene expression in the euryhaline tilapia (Oreochromis mossambicus) hypothalamic or environmental?
We examined the effects of environmental salinity on circulating levels of the two prolactins (tPRL177 and tPRL188) and levels of pituitary tPRL177 and tPRL188 mRNA in the euryhaline tilapia, Oreochromis mossambicus. Fish were sham-operated or hypophysectomized and the rostral pars distalis (RPD) autotransplanted onto the optic nerve. Following post-operative recovery in (1/4) seawater, tilapia were transferred to fresh water (FW), (1/4) seawater (SW) or SW. Serum tPRL177 and tPRL188 levels in sham-operated and RPD-autotransplanted fish were highest in FW and decreased as salinity was increased. tPRL177 and tPRL188 mRNA levels in RPD implants as well as in pituitaries from the sham-operated fish were also highest in FW and decreased with increasing salinity. Serum osmolality increased with salinity, with the highest levels occurring in the seawater groups. We conclude that some plasma factor (probably plasma osmolality), in the absence of hypothalamic innervation, exerts a direct regulatory action on prolactin release and gene expression in the pituitary of O. mossambicus. This regulation is in accord with the actions of the two prolactins in the freshwater osmoregulation of the tilapia. (+info)
(4/770) Does androgen insufficiency cause lacrimal gland inflammation and aqueous tear deficiency?
PURPOSE: The current investigators have shown that androgen treatment suppresses inflammation and stimulates the function of lacrimal glands in mouse models of Sjogren's syndrome. Recently, others have hypothesized that androgen insufficiency induces an autoimmune process in lacrimal tissue, leading to inflammation, a Sjogren's syndrome-like pathology, and aqueous tear deficiency. The purpose of the present study was to test this hypothesis. METHODS: Lacrimal glands were obtained from adult testicular feminized (Tfm) and control mice; castrated rats, guinea pigs, and rabbits; and castrated rats without anterior or whole pituitary glands and were processed for histology and image analysis. Tear volumes were measured in mice, in patients taking antiandrogen medications, and in age-matched human control subjects. RESULTS: Tfm mice, which are completely resistant to classical androgen action, did not have increased lymphocyte infiltration in their lacrimal glands or decreased tear volumes. No inflammation was evident in lacrimal tissues of male or female rats, guinea pigs, or rabbits 12 to 31 days after castration, no inflammation existed in rat lacrimal glands 15 to 31 days after orchiectomy and pituitary removal, and no aqueous tear deficiency was apparent in patients receiving antiandrogen therapy. CONCLUSIONS: Androgen deficiency may promote the progression of Sjogren's syndrome and its associated lacrimal gland inflammation, meibomian gland dysfunction, and severe dry eye. However, androgen insufficiency alone does not cause lacrimal gland inflammation, a Sjogren's syndrome-like pathology in lacrimal tissue, or aqueous tear deficiency in nonautoimmune animals and humans. (+info)
(5/770) Measurement of biological activity of somatotropin in hypophysectomized rats.
AIM: To develop a method for measurement of biological activity of recombinant DNA-derived somatotropin (rhGH). METHODS: The effects of varying the route, frequency and period of administration of GH, the sex of test animals on the biological responses, body weight gain (BWG), and tibial epiphyseal width (TEW), of hypophysectomized (Hypox) rats were compared, respectively. 4-d BWG, 6-d BWG, and 6-d TEW tests were carried out simultaneously in the same group of Hypox rats to determine the biopotency of GH preparations according to a parallel line bioassay (6-point assay). The final result was chosen from the test which had smaller values for the index of precision (lambda) and the average rate of fiducial limits (ARFL) than other tests. RESULTS: No significant differences in the responses between male and female rats, between sc and im, once daily and twice daily injections of bGH were found. But the BWG and TEW of Hypox rats injected with 0.045 and 0.135 IU.d-1 of bGH for 6 d were significantly greater than that for 4 d. Both 4-d BWG test and 6-d BWG test in the range from 0.020 to 0.500 IU.d-1 had values for lambda = 0.0660 and 0.1747, and for r = 0.9000 and 0.9237, respectively. Three estimates of rhGH preparation compared with the International Standard for somatotropin (IShGH), 4.6132, 3.9829, and 4.8023 IU/ampoule, were obtained separately from 4-d BWG test, 6-d BWG test and 6-d TEW test. And the result from 6-d BWG test was reported finally because it had smaller values for lambda and ARFL (0.0608 and 37.907%) than other two tests. CONCLUSION: Both BWG test and TEW test can be carried out simultaneously in the same group of Hypox rats. 6-d BWG test seemed to be more suitable for potency determination of GH preparations than 4-d BWG test and 6-d TEW test. (+info)
(6/770) Postnatal ontogeny and hormonal regulation of sulfotransferase SULT1B1 in male and female rats.
The ontogenic and hormonal regulation of a sulfotransferase, SULT1B1, was examined. Hepatic RNA was isolated from rats of various ages from 1 to 90 days. The mRNA for SULT1B1 is low for both sexes until a dramatic increase ( approximately 6-fold) occurs between 15 and 30 days of age in male rats. SULT1B1 expression then decreases to half of the maximal level by 90 days of age. The increase in SULT1B1 mRNA in female rats is less dramatic and occurs between 30 and 45 days of age. SULT1B1 mRNA expression plateaus from 45 to 90 days in female rats. Expression of SULT1B1 mRNA is comparable in adult male and female rats. RNA was isolated from hypophysectomized (HX) animals and HX animals treated with growth hormone [by either male (injection) or female (infusion) pattern], estradiol, progesterone, or testosterone. HX and HX plus growth hormone, or HX plus steroid replacement, did not alter SULT1B1 mRNA expression. Pituitary-intact rats were treated with steroidal compounds dexamethasone (DEX) and pregnenolone-16alpha-carbonitrile (PCN). Both DEX and PCN increased expression of SULT1B1 mRNA in male rats (4- and 3-fold, respectively). However, in female rats, only PCN induced SULT1B1 mRNA (2-fold), whereas DEX did not induce SULT1B1 in female rats. Analysis of SULT1B1 protein expression indicated that only when SULT1B1 mRNA was markedly increased, that is in DEX-treated male rats, was SULT1B1 protein increased. Thus, although adult male and female rats have similar SULT1B1 mRNA expressions, the patterns develop ontogenically differently. SULT1B1 is not regulated by pituitary hormones and DEX induces SULT1B1 protein in male rats. (+info)
(7/770) Cushing's disease masking coincidental steroid-responsive diseases.
Two cases of Cushing's disease are presented. In both cases successful treatment was followed by the development of a steroid-responsive disease condition, a seronegative arthritis in the first case and retinal vasculitis in the second. It is likely that both these conditions were unmasked by the fall in the endogenous steroid levels following the successful treatment of the Cushing's disease by trans-sphenoidal hypophysectomy. (+info)
(8/770) Glucocorticoids stimulate the accumulation of lipids in the rat corpus luteum.
We investigated the physiological basis for the trophic effect of glucocorticoids in rat corpora lutea in the absence of pituitary gonadotropins. Immature (Day 29) Sprague-Dawley rats were given eCG and hCG to induce the development of corpora lutea and were hypophysectomized on Day 32. Beginning on Day 40, rats received twice-daily s.c. injections of either dexamethasone (dex; 200 microg/rat/day) or vehicle (controls) and then were killed on Day 44. Plasma 20alpha-dihydroprogesterone, a major steroid produced by the corpora lutea, was higher (p = 0.01) in dex-treated than in control rats (44.5 +/- 2.3 vs. 23.0 +/- 5.6 ng/ml). Dexamethasone treatment increased lipid droplets and lipid in the corpora lutea as revealed by electron microscopy and oil red O staining. Cholesterol esters were higher in corpora lutea of dex-treated rats compared to controls (14.8 +/- 1.1 vs. 2.2 +/- 0.5 microg/mg corpora lutea wet tissue, respectively; p = 0.05). Another group of hypophysectomized rats was treated with either a high or a lower dosage of corticosterone, both of which caused an elevation to > 2-fold of plasma 20alpha-dihydroprogesterone concentration compared to controls. Glucocorticoid receptor protein (about 92 kDa) was detected in both luteal and nonluteal ovarian tissues in this animal model. These effects of glucocorticoids and the presence of the glucocorticoid receptor raise the possibility of a physiological role for glucocorticoids in the rat corpus luteum. (+info)