UNIPROT:P01189 - FACTA Search

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Query: UNIPROT:P01189 (beta-endorphin)
21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Following adrenalectomy (ADX), corticotropin-releasing factor (CRF) and vasopressin immunoreactivity are jointly expressed by a population of parvocellular neurosecretory neurons in the paraventricular nucleus of the hypothalamus (PVH). Because these cells stain positively for CRF, but not for vasopressin, after pretreatment with colchicine, the results suggest the existence of state-dependent alterations in the expression of peptides by neuroendocrine neurons. The present study sought to determine whether other neuropeptides (e.g., neurotensin, met-enkephalin) that have been colocalized with CRF in the parvocellular division of the PVH are influenced similarly by ADX; whether the enhancement of CRF and/or vasopressin immunoreactivity after ADX is limited to neurons of the PVH; and what factors might be involved in the regulation of the expression of these peptides in the PVH. The results confirmed that CRF and vasopressin immunoreactivity are both enhanced, and may be colocalized in a substantial population of parvocellular neurosecretory neurons after ADX; no comparable enhancement of staining for met-enkephalin or neurotensin was observed. The effect of ADX on CRF immunoreactivity was not limited to cells in the PVH, as neurons in the cerebral cortex, amygdala, and the bed nucleus of the stria terminalis also showed heightened CRF immunostaining after ADX; vasopressin immunoreactivity was never colocalized with CRF in these extrahypothalamic sites. Hypophysectomy produced an enhancement of CRF and vasopressin staining in the PVH that was comparable to that seen after ADX, implicating adrenal steroids as primary regulators of peptide expression in this system. Corticosteroid replacement studies in ADX rats indicated that lower doses of dexamethasone attenuated, and higher doses essentially abolished, the expected enhancement of both CRF and vasopressin immunoreactivity after ADX. The relative potency of steroids in mitigating these effects was dexamethasone greater than corticosterone greater than deoxycorticosterone greater than aldosterone. Collectively, these results indicate that the ADX-induced enhancement of CRF and vasopressin immunoreactivity in parvocellular neurosecretory neurons is at least somewhat specific to these peptides and to this cell type. Both peptides would appear to be regulated similarly by adrenal steroids, with glucocorticoids playing a primary role.
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PMID:Adrenalectomy-induced enhancement of CRF and vasopressin immunoreactivity in parvocellular neurosecretory neurons: anatomic, peptide, and steroid specificity. 355 42

Ten-week-old female obese and lean Zucker rats were given access to three separate macronutrient sources (casein, starch, and lard) for 7 days. They were then either adrenalectomized (ADX) or given a sham operation. Rats were assigned to one of three groups and given a daily injection of either 0, 2, or 10 mg of corticosterone. They continued to select a diet for another 17 days, after which they were killed, and their blood was assayed for corticosterone, adrenocorticotropin hormone (ACTH), insulin, glucose, and triglyceride. Retroperitoneal and parametrial fat depots were excised and sampled for lipoprotein lipase activity, fat cell size, and number. Body composition was also determined. Selection patterns of lean and obese rats were markedly affected by both ADX and corticosterone replacement. All three groups of sham-operated obese rats ate significantly more fat than did sham-operated lean rats. Adrenalectomy significantly reduced fat intakes in both obese and lean rats. Corticosterone therapy restored fat appetites of lean and obese rats in a dose-dependent fashion. In comparison to ADX lean rats, ADX obese rats reduced their normally elevated levels of blood glucose, plasma triglycerides, and insulin to within normal limits. Similarly, adipose cellularity of the ADX obese rats was reduced to that of sham-operated lean rats. Carcass fat was significantly reduced after adrenalectomy. Corticosterone therapy prevented the reduction in a dose-dependent way.
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PMID:Some metabolic and behavioral effects of adrenalectomy on obese Zucker rats. 377 20

The long term effect of adrenocorticotropin (ACTH) on the synthesis of adrenodoxin in bovine adrenocortical cells was investigated. Primary, confluent monolayer cultures of adult bovine adrenocortical cells were incubated in the presence or absence of ACTH (10(-6) M) for periods up to 72 h. The amount of adrenodoxin precursor synthesized in a cell-free translation system programmed with RNA isolated from ACTH-treated cells increased to approximately 3 times the control level by 36 h. Similarly, ACTH increased the rate of incorporation of [35S]methionine into mature adrenodoxin in radiolabeled adrenocortical cells, an effect that was maximal 36 h after initiation of ACTH treatment. At longer times (48-72 h), the stimulatory effect of ACTH was not maintained, and adrenodoxin synthesis in both radiolabeled cells and cell-free translation systems declined to control levels. The content of adrenodoxin in cells treated with ACTH for 36 h, as measured by electron paramagnetic resonance spectroscopy, was approximately twice that in control cells. The results indicate that ACTH induces the synthesis of adrenodoxin in bovine adrenocortical cells. Based on the present results as well as those previously reported with respect to the induction of cholesterol side chain cleavage cytochrome P-450 by ACTH (DuBois, R. N., Simpson, E. R., Kramer, R. E., and Waterman, M. R. (1981) J. Biol. Chem. 256, 7000-7005), it is proposed that the synthesis of the mitochondrial components of the adrenocortical steroid hydroxylase system is controlled by ACTH in a coordinate fashion.
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PMID:Adrenodoxin biosynthesis by bovine adrenal cells in monolayer culture. Induction by adrenocorticotropin. 618 68

In addition to its stimulatory effects on steroidogenesis, adrenocorticotropic hormone (ACTH) also has a trophic action on the adrenal cell. This is manifested in part by increases in the levels of key mitochondrial steroidogenic enzymes. The mechanism by which this trophic action of ACTH occurs has been studied in monolayer cultures of mouse adrenal cortical tumor cells. ACTH treatment of these cells stimulates the relative incorporation of amino acids into at least eight specific proteins in mitochondrial preparations. Two of these ACTH-responsive proteins are among the nine major adrenal polypeptides that fulfill the criteria of mitochondrial translation products: (i) their synthesis in intact cells is specifically resistant to inhibition by cycloheximide yet uniquely sensitive to chloramphenicol and (ii) they are synthesized in vitro by isolated mitochondria. The other six ACTH-responsive proteins are within the much larger category of mitochondrial proteins that are synthesized on cytoplasmic ribosomes. One of the proteins synthesized in the cytoplasm electrophoretically comigrates with purified beef adrenodoxin reductase and another with beef adrenodoxin. These findings indicate that ACTH regulates the synthesis (and turnover, or both) of specific mitochondrial proteins that are synthesized inside as well as outside the mitochondria of these adrenal cells.
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PMID:Adrenocorticotropic hormone increases specific proteins of the mitochondrial fraction that are translated inside or outside this organelle in cultured adrenal tumor cells. 625 35

Median eminence corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) and pituitary and peripheral plasma adrenocorticotropin (ACTH) and AVP were measured in male Wistar rats 1 and 2 weeks after bilateral adrenalectomy (ADX), sham operation (SHAM) or dexamethasone-treatment (DEX). Median eminence AVP content was unchanged 1 week after ADX but was significantly elevated 2 weeks after ADX, whereas CRF activity was reduced at 1 week after ADX and returned to control range at 2 weeks. Anterior pituitary ACTH content was elevated but posterior pituitary AVP content was reduced at 1 and 2 weeks after ADX. Plasma ACTH was greatly elevated in ADX rats and reduced in DEX rats, whereas plasma AVP did not differ significantly between these two groups or the control group. When ADX and SHAM rats were laparotomized under ether, plasma ACTH increased greatly, but this elevation was prevented by DEX treatment. The plasma AVP level was elevated in all three groups 2.5 min after onset of stress but returned to the basal range at 20 min. Median eminence CRF and AVP and pituitary ACTH and AVP were not significantly changed after onset of stress. These results indicate that the vasopressin and CRF-ACTH responses were not consistent in the median eminence, pituitary and peripheral plasma and suggest that vasopression is not involved in the feedback and acute stress mechanism of CRF-ACTH secretion. However, we have to measure CRF activity and AVP concentration in the hypophysial portal blood to confirm this conclusion.
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PMID:Vasopressin and CRF-ACTH in adrenalectomized and dexamethasone-treated rats. 625 47

The long term action of cyclic AMP analogs to stimulate the synthesis of cytochromes P-450scc, P-45011 beta, and adrenodoxin has been studied utilizing confluent monolayers of adult bovine adrenocortical cells maintained for periods of time up to 72 h in the absence or presence of dibutyryl cyclic AMP (1 mM), 8-bromo cyclic AMP (1 mM), or ACTH (adrenocorticotropin) (10(-6) M). The synthesis of these proteins was examined by radiolabeling cellular proteins with [35S]methionine or else by translating RNA extracted from such cells in a cell-free system in the presence of [35S]methionine. In each case, the protein under study was immunoprecipitated utilizing specific antisera, or IgG fractions prepared from such antisera. ACTH and both analogs of cyclic AMP caused an increase in the synthesis of cytochrome P-450scc which reached a maximum 36-48 h after addition, and then declined. On the other hand, butyric acid (1 mM) had no effect on the synthesis of cytochrome P-450scc. Cytochrome P-450scc activity measured as pregnenolone production by both intact cells or isolated mitochondria from such cells was increased following incubation of cells with either dibutyryl cyclic AMP or ACTH. The binding of rabbit anti-cytochrome P-450scc IgG was also increased in cells incubated with dibutyryl cyclic AMP or ACTH as estimated by immunofluorescence microscopy using fluorescein-tagged anti-rabbit IgG. Furthermore, dibutyryl cyclic AMP and ACTH both increased the synthesis of adrenodoxin and of cytochrome P-45011 beta, as well as the activity of 11 beta-hydroxylase. In addition, ACTH stimulated the secretion of cyclic AMP in a time- and concentration-dependent fashion. Thus, it is concluded that analogs of cyclic AMP can mimic the long term actions of ACTH to induce the synthesis of steroidogenic enzymes, and that this action of ACTH is likely mediated by cyclic AMP.
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PMID:Induction of synthesis of mitochondrial steroidogenic enzymes of bovine adrenocortical cells by analogs of cyclic AMP. 631 83

To further elucidate the mechanisms by which ACTH (adrenocorticotropin) exerts its long-term action to maintain normal levels of adrenocortical cytochromes P-450 and related enzymes, the abilities of cholera toxin and prostaglandins E2 and F2 alpha to induce the synthesis of cytochromes P-450scc, P-45011 beta, and P-450C21 and adrenodoxin have been examined. These effectors stimulate the production of cyclic AMP and thus steroidogenesis in the adrenal cortex. Using bovine adrenocortical cells in primary monolayer culture, we have shown that treatment with cholera toxin results in increased synthesis of cytochromes P-450scc and P-45011 beta and adrenodoxin, similar to the effect observed upon ACTH treatment. Prostaglandins E2 and F2 alpha are less effective at inducing the synthesis of the mitochondrial cytochromes P-450, and do not seem to induce the synthesis of adrenodoxin. Furthermore, cholera toxin was found to be less effective at inducing the synthesis of microsomal cytochrome P-450C21 than ACTH, and no more effective than the prostaglandins. Thus, while it appears that elevation of cyclic AMP levels is a necessary step leading to increased synthesis of adrenocortical forms of cytochrome P-450, the detailed mechanism of this induction will be found to be different for each of the different enzymes.
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PMID:Induction of synthesis of bovine adrenocortical cytochromes P-450scc, P-45011 beta, P-450C21, and adrenodoxin by prostaglandins E2 and F2 alpha and cholera toxin. 632 96

To study whether hemorrhage stimulates interleukin-6 (IL-6) production in conscious rats, 30% of the total blood was withdrawn over 3 min through an indwelling venous catheter and the shedblood was reinfused 1 h later. Plasma adrenocorticotropic hormone (ACTH), corticosterone and IL-6 concentration rapidly increased. Plasma ACTH levels peaked at 10 min and corticosterone and IL-6 peaked at 60 min; all started to decrease after reinfusion. In adrenalectomized (ADX) rats with or without a corticosterone pellet implant, there was an inverse relationship between IL-6 and corticosterone concentrations, greatest in ADX rats and lowest in ADX rats in which plasma corticosterone was elevated by crushing the implanted pellet. However, the ADX rats in which plasma corticosterone was maintained at normal or slightly elevated levels showed greater IL-6 responses to hemorrhage and elevated basal plasma IL-6 levels compared to sham-operated control rats. Twenty-four hours after hemorrhage/reinfusion, ACTH, corticosterone, and IL-6 responses to i.v. injection of lipopolysaccharide (LPS) were all reduced compared to the non-hemorrhaged animals, indicating that hemorrhage impaired general host defense. Although very high plasma corticosterone concentrations markedly suppressed the IL-6 response to LPS, in ADX rats in which plasma corticosterone was maintained at slightly higher levels than normal, the reduced IL-6 response to LPS in the posthemorrhage period was not reversed, but enhanced. Thus corticosterone has biphasic effects on the IL-6 response to hemorrhage and the response to LPS during the posthemorrhage period, which has important clinical implications with regard to the optimal dose of glucocorticoid for maintaining the host defense response.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Rapid increase in plasma IL-6 after hemorrhage, and posthemorrhage reduction of the IL-6 response to LPS, in conscious rats: interrelation with plasma corticosterone levels. 748 23

Hypothalamic-pituitary-adrenal (HPA) responses remain intact or increase after chronic or repeated stress despite robust levels of circulating glucocorticoids that would be expected to restrain the responsiveness of the axis. The purpose of this study was to determine whether chronic stress altered corticosteroid receptor messenger RNA (mRNA) levels at any locus known to mediate glucocorticoid feedback on HPA function (i.e. hippocampus or hypothalamus), whether such effects were glucocorticoid dependent, and whether changes in corticosteroid receptor function could potentially contribute to the putative shift from corticotropin-releasing hormone (CRH) to arginine vasopressin (AVP) in the hypothalamic paraventricular nucleus (PVN) in the modulation of pituitary adrenal function occurring during chronic stress. We compared the stress responsiveness of sham-operated rats to that of adrenalectomized rats using a moderate dose of corticosterone (CORT) pellet replacement (ADX + CORT group). Acute immobilization caused a significant increase in CRH, but not AVP, mRNA levels in the parvocellular PVN in sham rats. The ADX + CORT group showed significantly greater increases in both CRH and AVP mRNA levels in the PVN compared to sham rats. These data indicate that PVN AVP mRNA levels are more sensitive to glucocorticoid negative feedback than are the levels of CRH mRNA. In repeated stress, the sham groups showed robust increases in PVN CRH and AVP mRNA levels despite high levels of plasma CORT. The rise in AVP mRNA levels was greater than that in CRH mRNA. Type II glucocorticoid receptor mRNA in the hippocampus and PVN was decreased in the repeatedly stressed sham group. These data suggest a decrease in the CORT negative feedback restraint of PVN CRH and AVP mRNA levels repeated stress and a persistence of relatively greater responsiveness of AVP mRNA levels to CORT negative feedback. After repeated stress in ADX+CORT rats, both PVN CRH and AVP mRNA levels showed robust responses, with a relatively greater increase in AVP mRNA. These data indicate that a CORT-mediated decrease in hippocampal and hypothalamic glucocorticoid receptor mRNA levels is not the only mechanism contributing to the maintenance of a robust HPA response after repeated stress. Similarly, we postulate that the relative shift from CRH to AVP in the PVN after repeated stress is mediated by both a greater sensitivity of AVP to CORT negative feedback and CORT-independent mechanisms.
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PMID:Increased expression of corticotropin-releasing hormone and vasopressin messenger ribonucleic acid (mRNA) in the hypothalamic paraventricular nucleus during repeated stress: association with reduction in glucocorticoid receptor mRNA levels. 762 64

These experiments tested the sensitivity of cortisol feedback on adrenocorticotropic hormone (ACTH) secretion in adult sheep. In series I, five bilaterally adrenalectomized (ADX) adult sheep were maintained on "low" (125 micrograms/h) or "high" (500 micrograms/h) intravenous cortisol replacement, and dose-response curves were obtained with corticotropin-releasing factor (CRF) and arginine vasopressin (AVP). CRF caused incremental increases in plasma ACTH at the low but not the high dose of cortisol. AVP was similarly ineffective in stimulating ACTH at the high dose of cortisol. However, in series II, where ADX animals were again maintained on low or high cortisol infusions, a combined infusion of CRF and AVP was able to stimulate a robust ACTH response during both steroid replacement regimens. These studies demonstrate that the pituitary represents a major site of steroid feedback in the sheep, with a relatively small increase in the concentration of cortisol, within the normal unstressed physiological range, being able to inhibit ACTH secretion in response to exogenous CRF and AVP. However, under these conditions, inhibition of ACTH release can be overcome by the combined action of CRF and AVP. Further studies in series III, concerned with the nature of glucocorticoid inhibition of AVP release, demonstrate that whereas exposure to maximal cortisol levels (5,000 micrograms/h) completely abolishes the ACTH response to severe hemorrhage (15 ml/kg over 15 min), AVP release is maintained, suggesting that the system controlling AVP release during hemorrhagic stress is less sensitive to the negative influences of glucocorticoids than is the system controlling ACTH release.
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PMID:Cortisol feedback in adrenalectomized adult sheep. 763 64

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