Showing papers on "Hypophysectomy published in 2004"

Multihormonal regulation of hepatic sinusoidal Ntcp gene expression.

Abstract: Bile acids are efficiently removed from sinusoidal blood by a number of transporters including the Na+-taurocholate-cotransporting polypeptide (Ntcp). Na+-dependent bile salt uptake, as well as Ntcp, are expressed twofold higher in male compared with female rat livers. Also, estrogen administration to male rats decreases Ntcp expression. The aims of this study were to determine the hormonal mechanism(s) responsible for this sexually dimorphic expression of Ntcp. We examined castrated and hypophysectomized rats of both sexes. Sex steroid hormones, growth hormone, thyroid, and glucocorticoids were administered, and livers were examined for changes in Ntcp messenger RNA (mRNA). Ntcp mRNA and protein content were selectively increased in males. Estradiol selectively decreased Ntcp expression in males, whereas ovariectomy increased Ntcp in females, confirming the importance of estrogens in regulating Ntcp. Hypophysectomy decreased Ntcp mRNA levels in males and prevented estrogen administration from decreasing Ntcp, indicating the importance of pituitary hormones. Although constant infusion of growth hormone to intact males reduced Ntcp, its replacement alone after hypophysectomy did not restore the sex differences. In contrast, thyroid hormone and corticosterone increased Ntcp mRNA in hypophysectomized rats. Sex differences in Ntcp mRNA levels were produced only when the female pattern of growth hormone was administered to animals also receiving thyroid and corticosterone. Thyroid and dexamethasone also increased Ntcp mRNA in isolated rat hepatocytes, whereas growth hormone decreased Ntcp. These findings demonstrate the essential role that pituitary hormones play in the sexually dimorphic control of Ntcp expression in adult rat liver and in the mediation of estrogen effects.

Effects of prolactin and growth hormone on plasma levels of lysozyme and ceruloplasmin in rainbow trout.

Abstract: In vivo and in vitro effects of prolactin (PRL) and growth hormone (GH) on plasma levels of lysozyme and ceruloplasmin were examined in the rainbow trout (Oncorhynchus mykiss). Hypophysectomy had no effect on the plasma lysozyme level. Implantation of PRL- or GH-containing cholesterol pellets increased the lysozyme level in a dose-related manner. After hypophysectomy and sham operation, plasma ceruloplasmin was elevated above the level in intact fish, suggesting inflammation caused by the surgery. PRL or GH treatment significantly attenuated the increased level of ceruloplasmin in the operated fish. Expression of lysozyme mRNA was detected in the leucocytes isolated from the peripheral blood by RT-PCR. In vitro administration of PRL or GH showed no effect on the proliferation of isolated leucocytes or on the total protein content; however, lysozyme activity in the medium increased in a dose-related manner. These results suggest that PRL and GH directly stimulate lysozyme production without affecting the proliferation of leucocytes, and the attenuated ceruloplasmin level increased in response to inflammation.

Allopregnanolone in the brain and blood after disruption of the hypothalamic-pituitary-adrenal axis in fetal sheep.

Abstract: Neuroactive steroids may be synthesised in the brain either de novo from cholesterol or from blood-borne precursors. Concentrations of a GABAA receptor agonist, allopregnanolone, in the fetal brain exceed those in the circulation, and are markedly higher than adult brain concentrations. We used fetal hypophysectomy or adrenalectomy to elucidate the contribution of hypothalamic-pituitary factors and adrenal steroid secretion to the overall neuroactive steroid level in both the fetal brain and the fetal circulation. Hypophysectomy or adrenalectomy was performed between 108 and 112 days of gestation (term approximately 147 days) and fetal tissues were collected at 140 days of gestation. Immunoreactive (ir) ACTH and cortisol in the plasma were significantly reduced after hypophysectomy, whereas adrenalectomy led to increased irACTH but significantly decreased cortisol concentrations, as expected. Brain concentrations of allopregnanolone, progesterone and pregnenolone did not change significantly in fetuses that underwent either hypophysectomy or adrenalectomy; however, concentrations in the plasma and content in the adrenal gland were decreased. Expression of cytochrome P450 scc and 5alpha-reductase type II (5alphaRII) in the brain, measured by western immunoblotting, did not change after either hypophysectomy or adrenalectomy but, after hypophysectomy, expression of P450 scc in the adrenal gland was significantly decreased and that of 5alphaRII remained unchanged. These findings suggest that the regulation of the neuroactive steroid content in the fetal brain is independent of adrenal steroidogenesis and hypothalamic-pituitary factors. Furthermore, the absence of a change in enzyme expression in the brain suggests that the control of the expression of these enzymes is independent of hypothalamic-pituitary factors. Thus local control mechanisms within the brain may be responsible for maintaining the high neurosteroid content present during fetal life, as these mechanisms are independent of adrenal steroid production.

An ex vivo analysis of Sertoli cell actin dynamics following gonadotropic hormone withdrawal.

Abstract: The receptors for the steroid hormone testosterone and the peptide hormone follicle-stimulating hormone are localized to the somatic Sertoli cell in the seminiferous epithelium. In the rat, prolonged gonadotrophic hormone withdrawal has been shown to result in substantial germ cell apoptosis. Previous studies have shown that, coincident with the loss of germ cells following hypophysectomy, the actin cytoskeleton of the Sertoli cell becomes disorganized and diffuse throughout the cell's cytoplasm. The molecular mechanisms that govern Sertoli cell actin filament dynamics in response to the loss of gonadotrophic hormones remain undefined. It was therefore hypothesized that hypophysectomy brings about a decrease in the amount of polymerized actin (F-actin) within the Sertoli cell and that this decrease is associated with changes in the expression of genes known to govern Sertoli actin dynamics. To this end, Sertoli cells were isolated from adult control and hypophysectomized rats. Sertoli cells from hypophysectomized rats were found to contain significantly less (72%) F-actin relative to untreated controls, although overall, β-actin protein and mRNA expression remained constant. The expression levels of genes known to directly influence the amount of F-actin in cells were then examined by Northern blot analysis. Cofilin and profilin I gene expression was unaffected by hypophysectomy, whereas the expression of profilin II and espin both decreased significantly (47% and 42%, respectively). Taken together, these results suggest that, following hypophysectomy, the actin cytoskeleton of the Sertoli cell shifts to a predominantly depolymerized state, perhaps in part because of decreases in profilin II and espin gene products.

Immunocytochemical localization of mK1, a true tissue kallikrein, in the mouse parotid gland: sexual dimorphism and effects of castration and hypophysectomy.

Abstract: In the normal parotid glands of mice at 12 weeks of age, mK1, a true tissue kallikrein, was detected at the apical rim of the striated ducts (SDs). Sexual dimorphism in the immunostaining intensity in parotid glands was seen, i.e., immunostaining was more intense in males than in females. Under electron microscopy, secretory granules, being small in size, and condensed at the subluminal cytoplasm, were labeled with immunogold particles showing the presence of mK1. These secretory granules were rather abundant and large in males. Castration in males reduced the immunoreactivity of mK1 in the SD cells because of a decrease in the number and size of secretory granules as revealed by electron microscopy. Hypophysectomy in male mice resulted in considerable loss of immunoreactivity for mK1, which was characterized under electron microscopy by complete disappearance or significant reduction of secretory granules in many SD cells. These results suggest that mK1 expression in the SD cells of murine parotid glands is regulated by pituitary-dependent hormones, and sexual dimorphism of mK1 expression is regulated by androgens.

Effects of hypophysectomy and in vivo administration of ACTH or dexamethasone on the level of ACTH receptor mRNA in adrenal glands and adipose tissues of mice.

Abstract: Objective In rodents, ACTH induces steroidogenesis in the adrenal cortex and also lipolysis in adipose tissues via the sole specific receptor for ACTH. Up-regulation of the ACTH receptor (ACTH-R) mRNA by ACTH was found to be evident in adrenocortical cells. However, a role of in vivo ACTH on ACTH-R mRNA expression in the adrenal cortex is not well understood. In addition, so far less attention has been also paid to the regulation of ACTH-R expression in adipose tissues. We investigated the effects of hypophysectomy and in vivo administration of ACTH or dexamethasone on the level of ACTH-R mRNA in the adrenal gland and adipose tissues of mice. Methods ACTH mRNA in the adrenal glands and epididymal adipose tissues of mice sacrificed 10 days after hypophysectomy or sham operation, and 24 hours after ACTH-Z (2 IU i.m.) or physiological saline solution (PSS) injection, and also 3-days after dexamethasone (300 microg/day i.m.) or PSS administration was analysed by Northern blot, and intensities of autoradiographic bands were quantified. Results In the adrenal gland, in vivo administration of ACTH-Z significantly increased the level of ACTH-R mRNA to 342% of control values, but in vivo administration of dexamethasone or hypophysectomy induced no significant alteration of ACTH-R mRNA. In adipose tissues, these conditions did not significantly alter the level of ACTH-R mRNA. Conclusion Low circulating ACTH may not be a substantial factor for ACTH-R gene expression in the adrenal gland, but a high level of in vivo ACTH dose up-regulated the expression. A different regulation of ACTH-R gene expression exists in the adrenal cortex and adipose tissues of mice.

The role of gap junctions in adrenal gland function

Abstract: This thesis explores the theory that gap junctions play a role in adrenocortical homeostasis and function. To test this hypothesis, gap junction mediated communication was investigated in the intact adrenal gland. In addition, to determine the impact of altered adrenal trophic state on gap junction distribution and expression, adrenal glands from hypophysectomized mice as well as normal and neoplastic human adrenal tissues were evaluated. Gap junction mediated intercellular communication was done in primary mouse adrenal glands using a modified Lucifer Yellow dye communication assay. Dye communication showed that the adrenal cortex was communication competent and that functional cell-cell communication was directly related to the abundance of connexin 43 expression. There was an absence of dye communication in the outer cortical zona glomerulosa (ZG) that was contrasted by a high level of communication in the inner zones of the zonae fasciculata/reticularis (ZF/ZR).The removal of the endogenous pituitary derived ACTH stimulus by hypophysectomy resulted in a significant loss of connexin 43 expression in the ZF/ZR that was associated with a diminished trophic state. The loss of connexin 43 expression was concurrent with features associated with a diminished functional state of the gland including loss of lipid droplets and reduced expression of the ZG specific cytochrome P450 aldosterone synthase (P450 aldo). A comparison of adrenal glands from connexin 43 deficient mice (Cx 43 -/-) demonstrated several features that were similar to those observed in hypophysectomized mice, including glandular atrophy and reduced P450 aldo expression in the ZG.Connexin 43 expression and distribution in the normal human adrenal gland was identical to that previously described in the adrenal glands from other mammals. Connexin 43 expression was abundant in the ZF/ZR and nearly absent from the parenchymal cells of the ZG. Immunocytochemial analysis of neoplastic tissues showed that benign (adenoma) and malignant (carcinoma) neoplasms lost 30% and 90% respectively, of their connexin 43 expression in the ZF/ZR when compared to normal tissues. The data presented here demonstrate that connexin 43 expression is related to physiological changes that affect adrenal trophic state and suggest that gap junction mediated cell-cell communication is involved in the function of the adrenal cortex. Furthermore, because connexin 43 deficient animals also exhibit glandular changes consistent with a diminished state of the adrenal gland, it supports a role for proper gap junction expression in adrenal cortex development and function.