Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In addition to reconstituting immune competence, the thymus gland preparation, thymosin fraction 5 (TSN-5), has recently been shown to stimulate secretion of hormones from the hypothalamic-pituitary adrenal axis in vivo and from pituitary corticotropes in vitro. The purpose of the present study was to investigate the effects of TSN-5 on secretion of immunoreactive beta-endorphin (i beta-E) by mouse corticotropic tumor cells. The release of i beta-E by AtT-20 pituitary tumor cells was increased in a dose-dependent manner by concentrations of 30-600 micrograms/ml of TSN-5, whereas concentrations greater than 1,000 micrograms/ml were increasingly less effective in stimulating secretion. TSN-5 (600 micrograms/ml) significantly stimulated i beta-E release within 7 min; maximal secretory responses (up to 275% of control release) occurred by 4 hr. The secretory response of AtT-20 cells to 600 micrograms/ml TSN-5 (37.9 +/- 2.0 vs. 16.1 +/- 1.0 ng i beta-E/ml/4 hr, mean +/- SE) was similar in magnitude to release evoked by 0.1 microM corticotropin-releasing factor (CRF). Combining TSN-5 and CRF treatments increased secretion of i beta-E to nearly 600% of control levels, an effect greater than an additive influence of the two independent treatments. Whereas CRF treatment reduced the levels of i beta-E in AtT-20 cell extracts after 24-hr treatment by 45% (231.8 +/- 24.7 vs. 417.2 +/- 17.8 ng i beta-E/mg protein, CRF vs. vehicle treatments, respectively), TSN-5 did not significantly alter cellular hormone content. Neither TSN-alpha 1 nor TSN-beta 4, two of the component peptides of TSN-5, affected basal or CRF-stimulated release of i beta-E, indicating that an unidentified constituent(s) is corticotropic.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thymosin fraction 5 stimulates secretion of immunoreactive beta-endorphin in mouse corticotropic tumor cells. 296 Aug 24

The involvement of calmodulin in the secretion of beta-endorphin from the mouse anterior pituitary tumor cell line, AtT-20, was investigated. The calmodulin inhibitor W7 potentiated secretion produced by 8-BrcAMP, and induced a secretory response to arginine vasopressin, which did not elevate beta-endorphin levels when added alone. Release of hormone in response to CRF was not affected. Calmodulin phosphodiesterase inhibitor 8-MeOMeMIX produced a dose-dependent increase in 8-BrcAMP stimulation, suggesting that inhibition of cAMP degradation is the mechanism of enhancement of 8-BrcAMP-induced secretion in the presence of W7.
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PMID:Modulation of beta-endorphin secretion from mouse pituitary tumor cells by calmodulin inhibitor W7. 296 20

The effects of the progesterone antagonist RU 38486 and the progesterone agonist megestrol acetate on the growth of the estrogen-progesterone receptor-positive transplantable adrenocorticotropin (ACTH)/prolactin-secreting rat pituitary tumor 7315a were examined. RU 38486 (2.5 mg/kg/day) for 30 days significantly inhibited tumor size, tumor weight, and the plasma prolactin and ACTH concentrations, while the same dose of megestrol acetate only inhibited pituitary tumor weight. Megestrol acetate inhibited both the release and total ACTH content of the anterior pituitary gland, while RU 38486 increased both the release and the total ACTH content. Studies with ACTH secretion by cultured normal rat pituitary cells showed that megestrol acetate (1 microM) did not affect corticotropin-releasing factor (CRF)-stimulated ACTH release after 4-hr exposure, but inhibited CRF-stimulated ACTH release by 50% after 24-hr preincubation. The glucocorticoid-like effect of 1 microM megestrol acetate in this model is similar to that exerted by 10 nM dexamethasone. Acute exposure or preincubation of rat pituitary cells with RU 38486 (1 microM) did not influence CRF-stimulated ACTH release, while preincubation for 24 hr revealed a dose-dependent reversing effect of RU 38486 on dexamethasone-induced inhibition of CRF-stimulated ACTH release. In this model, 1 microM RU 38486 completely overcame the effect of 10 nM dexamethasone. Megestrol acetate and RU 38486 have inhibitory effects on the growth of the 7315a tumor. They differ both with regard to their effects on the progesterone and the glucocorticoid receptor, with megestrol acetate exerting an agonistic and RU 38486 an antagonistic action.
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PMID:Comparison of the actions of RU 38486 and megestrol acetate in the model of a transplantable adrenocorticotropin- and prolactin-secreting rat pituitary tumor. 298 81

Isolated adrenocorticotropic hormone (ACTH) deficiency was documented after cesarean delivery in a patient with type I diabetes. A preceding severe headache, subsequent declining insulin requirements, and hypotension are consistent with pituitary infarction in a patient without computed tomography evidence of a pituitary tumor. Antepartum incomplete pituitary infarction with isolated ACTH deficiency is an unusual but potentially catastrophic complication of the pregnant diabetic.
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PMID:Isolated adrenocorticotropic hormone deficiency with antepartum pituitary infarction in a type I diabetic. 298 76

A mouse pituitary tumor cell line (AtT-20) releases corticotropin (ACTH) in response to a number of secretagogues, including corticotropin-releasing factor (CRF), beta-adrenergic agents, N6,O2'-dibutyryladenosine 3',5'-cyclic monophosphate (Bt2 cAMP), and potassium. The stimulation of ACTH secretion induced by the secretagogues can be blocked by inhibitors of the enzymes that generate (phospholipase A2) and metabolize (lipoxygenase and epoxygenase) arachidonic acid. The phospholipase A2 blockers mepacrine and p-bromophenacylbromide inhibited the ACTH release induced by secretagogues. The lipoxygenase inhibitors nordihydroguaieretic acid, butylated hydroxytoluene, and icosatetraynoic acid abolished the ACTH secretion induced by secretagogues, whereas indomethacin, a cycloxygenase inhibitor, did not. Blockers of the cytochrome P-450 epoxygenase, such as SKF 525A and piperonyl butoxide, compounds that have different molecular structures, also suppressed secretagogue-induced ACTH release. These findings suggest that metabolites of arachidonic acid formed via the epoxygenase and/or the lipoxygenase pathway are involved in the stimulation of ACTH release caused by secretagogues.
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PMID:Inhibitors of the cytochrome P-450 enzymes block the secretagogue-induced release of corticotropin in mouse pituitary tumor cells. 298 24

Lithium stimulated corticotropin (ACTH) secretion by mouse pituitary tumor cells (AtT-20/D16-16) and by normal rat anterior pituitary cells in primary culture. Effects were observed at less than 2 mM LiCl. ACTH secretion was comparable in magnitude to that induced by other secretagogues, was calcium dependent, and was inhibited by somatostatin. Lithium also induced changes in [3H]inositide metabolism; these changes accompanied and were correlated with changes in ACTH secretion. The most prominent and reliable effect was to increase [3H]inositol monophosphate. Other secretagogues had no effect on [3H]inositides in the presence or absence of lithium. Pretreatment with lithium for 3 hr desensitized the cells to the effects of subsequent exposure to lithium. The cells were not desensitized to lithium by pretreatment with other secretagogues, nor were they desensitized by lithium to the effects of corticotropin-releasing factor, high potassium, or forskolin. However, pretreatment with lithium did desensitize the cells to stimulation by phorbol esters. The interaction between lithium and phorbol esters suggests the involvement of inositide metabolism and protein kinase C in the regulation of ACTH secretion and possibly of other hormones or neurotransmitters. It also suggests new avenues of research into the basis of lithium's psychopharmacological effects.
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PMID:Lithium induces corticotropin secretion and desensitization in cultured anterior pituitary cells. 298 36

Cushing's syndrome is the consequence of a sustained overproduction of cortisol (hydrocortisone) by the adrenal cortex. This may be due to excessive secretion of cortisol by functioning adrenocortical tumors or to "nontumorous" adrenocortical hyperfunction. The latter may be a result of stimulation of the adrenal cortex by increased release of corticotropin (ACTH) from a small pituitary tumor or from nonpituitary nonadrenal tumor. Carcinoids or carcinomas of the lung or pancreas, and even pheochromocytomas have caused the syndrome of ectopic ACTH production. The problems involved in the diagnosis of Cushing's syndrome are establishing its presence and determining the underlying cause. Treatment is then dependent upon the underlying pathogenetic lesion.
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PMID:Diagnosis and pathophysiology of Cushing's syndrome. 300 1

Molecular forms of immunoreactive adrenocorticotropin (ACTH), beta-lipotropin (beta-LPH) (beta-endorphin (beta-END), human NH-2-terminal (hNT) of pro-opiomelanocortin (POMC), and gamma-3-melanotropin (gamma-3-MSCH) were studied in plasma, CSF and urine of a patient with Nelson's syndrome by molecular sieving and concanavalin A (Con A)-sepharose chromatography. In the culture tumor medium of the tumor cells, and in the plasma and CSF, these compounds were found mainly in forms corresponding in molecular weight to the authentic peptides, with the exception of gamma-3-MSH. Stimulation of the pituitary tumor by synthetic ovine corticotropin-releasing factor (CRF 1-41) caused a 171-468% increase in vivo (60 min) and 453-953% increase in vitro (3h incubation) in the levels of POMC derived peptides; it increased the relative amount of beta-END in vivo, and that of beta-LPH in vitro. Molecular sieving chromatography of urine samples revealed that beta-LPH and hNT are extensively degraded by the kidney. By contrast, ACTH showed no significant renal degradation before the removal of the pituitary adenoma. However, following pituitary surgery, only smaller fragments of immunoreactive (IR) ACTH were detected in the urine. These results suggest no major abnormal metabolic pathway for POMC in Nelson's syndrome, although the proportions of various peptides derived from the precursor could be different in vivo from those after in vitro incubation under basal conditions and during CRF stimulation. The results also indicate differences in the renal handling of ACTH in POMC hypersecretory states.
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PMID:Characterization of peptides derived from pro-opiomelanocortin in the biological fluids of a patient with Nelson's syndrome. 300 68

Previous studies have shown that phorbol esters and lithium each stimulate the secretion of adrenocorticotropic hormone (ACTH) by the anterior pituitary tumor cell line AtT20/D16-16. Pretreatment with either lithium or phorbol ester desensitizes the cells to subsequent stimulation by phorbol ester. An early consequence of phorbol ester action in other systems is the translocation of protein kinase C from cytosol to membranes. We have assayed protein kinase C activity in cytosol and membranes of AtT20 cells after treatment with phorbol dibutyrate, lithium, or other agents that stimulate secretion of ACTH in these cells. Phorbol dibutyrate clearly induced translocation of protein kinase C, but lithium treatment did not cause translocation itself, nor did pretreatment with lithium affect the translocation induced by phorbol dibutyrate. These results are consistent with a role for translocation of protein kinase C in the stimulatory and desensitizing effects of phorbol esters but fail to implicate translocation in the actions of lithium on AtT20 cells.
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PMID:Translocation of protein kinase C in anterior pituitary tumor cells. 302 60

Anterior pituitary hypersecretion can be due to abnormal hypothalamic regulation, decreased peripheral hormone feedback or pituitary tumor. In some cases hypersecretion gives rise to a typical clinical syndrome involving acromegaly, hyperprolactinemia, and excess corticotropin (ACTH). The etiology of acromegaly is a growth hormone (GH)-secreting pituitary tumor in the vast majority of cases. Hyperprolactinemia and excess cortisol, however, may be due to many causes among which prolactin (PRL)- and ACTH-secreting pituitary tumors are not frequent. Glycoprotein-secreting pituitary tumors, especially gonadotropin (LH and FSH) and free subunits usually do not cause a typical excess hormone syndrome. Perhaps for this reason they are seldom recognized clinically, although histopathological studies are increasingly disclosing the gonadotrope nature of many pituitary tumors. Mixed hormonal secretions are common. When pituitary hormone secretion can be selectively suppressed by medical therapy, a significant reduction of tumor size is by no means rare. In other cases, pituitary irradiation or surgery, or even treatment aimed at a peripheral target gland, may be necessary.
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PMID:[Anterior pituitary hypersecretion syndromes]. 302 61


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