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)

We have studied the effects of 30 peptides administered intracerebroventricularly on basal and pentagastrin-stimulated (8 micrograms/kg s.c.) gastric acid secretion in conscious dogs. None of the peptides significantly increased basal gastric acid secretion. Twelve peptides (2 nmol/kg) significantly (p less than 0.01) decreased the pentagastrin-stimulated 2-h acid output (percentage inhibition in parentheses): human calcitonin (CT) (36%), neurotensin (NT) (52%), rat corticotropin-releasing factor (CRF) (59%), human calcitonin gene-related peptide (CGRP) (59%), ovine CRF (66%), beta-endorphin (beta-End) (80%), urotensin-I (81%), rat CT (81%), porcine gastrin-releasing peptide (GRP) (83%), sauvagine (Svg) (85%), rat CGRP (87%), and bombesin (Bom) (95%). Blockade of the autonomic nervous system with chlorisondamine abolished the gastric inhibitory action induced by CRF, beta-End, CT, and NT, but not by CGRP and Bom (1 nmol/kg each). Corticotropin-releasing factor, beta-End, CT, NT, CGRP, and Bom significantly inhibited gastric acid secretion stimulated by an intragastric 8% peptone meal for 2 h. None of these six peptides significantly altered plasma gastrin concentrations in response to the peptone meal as compared with control experiments. A rise of plasma concentrations of gastrin, CT, CRF, and CGRP could not be detected by radioimmunoassay in animals after intracerebroventricular administration of these four peptides. The results of this study indicate that CT, CGRP, NT, beta-End, and peptides of the CRF and Bom families act within the brain to inhibit pentagastrin- and meal-stimulated gastric acid secretion in conscious dogs. None of the 30 peptides administered intracerebroventricularly increased basal gastric acid secretion in the dog. Inhibition of gastric acid secretion induced by CRF, beta-End, CT, and NT, but not by CGRP and Bom is mediated by the autonomic nervous system. Gastrin does not appear to play a role in gastric acid inhibition induced by the six brain peptides studied.
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PMID:Inhibition of gastric acid secretion by brain peptides in the dog. Role of the autonomic nervous system and gastrin. 294 29

The effect of synthetic eel calcitonin (CT) on the level of plasma beta-endorphin-like immunoreactivity (beta-En-LI) and on its content in hypothalamus and anterior pituitary in vivo and on the release of beta-En-LI-from anterior pituitary in vitro was studied. The level of beta-En-LI was increased significantly in a dose-dependent manner after the injection of 1-100 U/kg CT, maximum level being found at 10 min after the injection. After the administration of 50 U/kg CT, the increase was still significant at 40 min. Such an increase was not found in hypophysectomized animals. The content of beta-En-LI in the hypothalamus and anterior pituitary did not change significantly after CT injection. In vitro, the release of beta-En-LI from anterior pituitary was enhanced significantly after CT. It may be concluded that CT acts on the pituitary to increase the release of beta-En-LI which results in increased plasma level.
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PMID:Effects of eel calcitonin on plasma beta-endorphin-like immunoreactivity levels in rats. 297 Mar 83

Neuroendocrine (NE) neoplasms of the human bronchopulmonary tract were examined by electron microscopy, immunocytochemistry, and gel electrophoresis of cytoskeletal proteins from microdissected tissue samples. All samples (carcinoids, well-differentiated NE carcinoma, NE carcinomas of intermediate type, NE carcinomas of the small cell type) contained significant numbers of cells that immunostained for one or more of the following neuroendocrine markers tested: bombesin, calcitonin, ACTH, leu-enkephalin, gastrin, serotonin, somatostatin, alpha-melanocyte-stimulating hormone, vasoactive intestinal peptide, glucagon, insulin, substance P, and neuron-specific enolase. Electron microscopy revealed typical NE cell features, including variable abundant and frequently heterogeneous neurosecretory granules. Tumor cells contained filaments specifically stained with different conventional and monoclonal antibodies to cytokeratins and displayed punctate plasma membrane staining with antibodies to desmoplakins, in agreement with the electron microscopic demonstration of tonofilament bundles and desmosomes. Immunocytochemistry for NE markers and cytoskeletal proteins on consecutive sections revealed both cytokeratins and neuroendocrine substances in single cells. Using gel electrophoresis of cytoskeletal proteins of tissue regions extracted with high salt buffer and detergent, we could detect, in the tumors tested, appreciable amounts of cytokeratin polypeptides 8, 18, and 19, i.e., major cytokeratins also found in certain other lung carcinomas such as adenocarcinomas. Tumor cells were not significantly stained with antibodies to other intermediate filament proteins such as vimentin, desmin, glial filament protein, and neurofilament protein. The results show that NE substances can be synthesized in cells containing a typical epithelial cytoskeleton, i.e., cytokeratin filaments and desmosomes. These findings support the notion of an epithelial character of these tumors and appear in contrast with recent reports that neurofilaments are the only type of intermediate filaments present in carcinoids and other pulmonary NE tumors. These observations may have important implications for the histogenesis of NE carcinomas and for diagnostic pathology.
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PMID:Coexpression of neuroendocrine markers and epithelial cytoskeletal proteins in bronchopulmonary neuroendocrine neoplasms. 298 72

A comparison was made with the data of 62 cases of pituitary adenoma, evaluated pre- and postoperatively, including as well the results of immunohistochemical hormone examination (also for calcitonin). Prolactin was found in 18 of the 21 adenomas carrying the preoperative diagnosis of prolactinoma, whereas cells containing other hormones (growth hormone, LH, FSH, TSH, ACTH, beta-endorphin), were only occasionally present. The growth hormone was strongly positive in the adenoma tissue in 16 of the 17 cases of acromegaly. 5 of these adenomas were accompanied by a marked hyperprolactinemia and also contained many prolactin cells. 6 of the 19 adenomas diagnosed as being 'inactive' contained hormone-positive cells, but only a very small number of cells. ACTH was found in 3 of the 4 pituitary adenomas of patients with Cushing's disease. 2 of these were also positive for beta-endorphin. The tissue of 1 gonadotrophic adenoma (with elevated FSH in serum) gave positive results with an anti-LH antiserum. Calcitonin was not found in any adenoma. The preoperative serum prolactin levels did not quantitatively correlate with the percentage of prolactin-positive cells.
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PMID:Immunohistochemical examination of pituitary adenomas. Comparison to clinical and endocrinological findings. 298 43

The most examined tumor markers in lung cancer patients are CEA, hormonal peptides, and some neurogenic enzymes in small cell carcinoma. Calcitonin, ACTH, ADH, CEA, neurophysin, oxytocin, beta-endorphin, neuron-specific enolase, and CK BB are elevated in serum specimens in 25-75% of cases of small cell carcinoma. The level of these markers is related to the stage of the disease in groups of patients; elevated pretreatment levels decrease with tumor regression. Marker levels are not valid in defining the tumor load and the presence of disease in the individual patient. It has not yet been documented that the markers can be used for clinical decisions on antineoplastic therapy. A recent development is the finding that measurement of CSF and plasma concentrations of ADH, calcitonin, CK BB, bombesin, and neuron-specific enolase may contribute in the diagnosis of CNS metastases including meningeal carcinomatosis.
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PMID:Tumor markers in patients with lung cancer. 300 40

The Saccharomyces cerevisiae secretory process was studied by evaluating secretion efficiency, processing efficiency, and the efficiency of protein folding for hybrid proteins containing the yeast prepro-alpha-factor leader region. Secretion of three proteins, beta-endorphin, calcitonin, and a consensus alpha-interferon (IFN-Con1), were compared in terms of secretion efficiency into the culture medium, beta-Endorphin and calcitonin, both small proteins, were found to be efficiently secreted from logarithmically grown cells. In contrast, the larger IFN-Con1 accumulated in the periplasmic space and cell wall. The glycosylated, unprocessed prepro-alpha-factor/IFN-Con1 fusion protein was also found to be secreted into the culture medium. The presence of (Glu-Ala) dipeptides in the alpha-factor spacer peptide increased the efficiency of cleavage at Lys-Arg in the prepro-alpha-factor/IFN-Con1 protein fusion. Purified secreted IFN-Con1 was structurally characterized to determine the effect of passage through the yeast secretory pathway on the fidelity and efficiency of protein folding. The disulfide structure of the secreted protein was found to be identical with that reported for the native human alpha-interferons.
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PMID:Protein secretion from Saccharomyces cerevisiae directed by the prepro-alpha-factor leader region. 300 32

The response of ACTH, beta-endorphin and cortisol to calcitonin administration was investigated in 8 subjects with recent fractures of the vertebrae due to postmenopausal or senile osteoporosis (Ost) and in seven normal healthy controls (NC). A significant increase of the three hormones was observed in 13 subjects. The maximum increase was observed between 15 and 60 min.: the cortisol level (microgram/100 ml) rose from 14.3 +/- 1.9 to 24.8 +/- 3.2 (P less than 0.05) in Ost and from 7.7 +/- 0.6 to 21.7 +/- 1.7 (P less than 0.001) in NC, the beta-endorphin (pmol/l) from 5.8 +/- 0.6 and to 21.2 +/- 1.3 in OST (P less than 0.001) and from 5.9 +/- 0.4 to 21.9 +/- 4.5 (P less than 0.01) in NC and the ACTH levels (pg/ml) from 21.3 +/- 5.7 to 61.7 +/- 3.6 (P less than 0.001) in OST and from 30.0 +/- 6.2 to 58.8 +/- 7.5 (P less than 0.05) in NC. The results indicate a possible role of calcitonin in modulating the anterior pituitary function. It also suggests that the analgesic effect of calcitonin might be mediated by the increase of beta-endorphin. The possibility that this analgesic effect of calcitonin is due to its direct binding to the opiate receptors was excluded in the present study by in vitro binding assay.
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PMID:Calcitonin induced increase in ACTH, beta-endorphin and cortisol secretion. 301 27

The present study was performed to investigate the potential of human medullary thyroid carcinoma (MTC) cells to secrete ACTH, beta-LPH/beta-EP. In addition, these studies might shed further light on the possible synthesis of a common precursor molecule for calcitonin (CT), ACTH and beta-LPH/beta-EP. MTC tissue was obtained from 10 patients (6 familial, 4 sporadic) without clinical and biochemical signs of Cushing's syndrome. Single cell suspensions were cultured for 1 to 2 weeks. Mean basal release of beta-LPH/beta-EP was 0.76 +/- 0.29 (SE) ng/10(6) cells/4 h (n = 10). Dibutyryl cyclic AMP (3 mM) stimulated beta-EP release significantly in 3 out of 7 cultures, while Ca2+ (2 mM) had no effect at all. The effects of the physiological regulators of pituitary ACTH and beta-LPH/beta-EP secretion, synthetic corticotropin-releasing factor (CRF-41) and vasopressin (LVP) were also studied in these MTC cell cultures. LVP (100 nM) had no effect on beta-EP release from MTC cells of all 8 cultures investigated. CRF-41 (10 nM) stimulated beta-EP release from 5 cultures and was without effect on 4. Maximal stimulation was noticed with 10 nM, while the effect of 100 nM CRF-41 was lower or absent. Stimulation was most outspoken in 3 cultures of familial MTC, whereas in 2 cultures of sporadic MTC CRF-41 stimulated beta-EP release marginally only after a 24 h incubation. LVP and/or CRF-41 stimulated CT release significantly in 3 cultures from sporadic MTC, while in these cultures the effect of CRF-41 on beta-EP release was either very small or absent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Secretion of adrenocorticotropin, beta-endorphin and calcitonin by cultured medullary thyroid carcinoma cells. Effects of synthetic corticotropin-releasing factor and lysine vasopressin. 302 Aug 52

Immunoreactivity for endocrine peptides (serotonin, gastrin, somatostatin, insulin, corticotropin, calcitonin, neurotensin, vasoactive intestinal peptide, and bombesin), cytoskeletal proteins (high and low molecular weight keratins), and tumor differentiation markers (chromogranin, neuron-specific enolase, carcinoembryonic antigen, S100 protein, and Grimelius stain) was sought on nine cervical and one vaginal poorly differentiated small-cell carcinoids. Dense-core secretory granules were ultrastructurally identified in all cases (seven of ten) in which tissue was available for electron microscopy. Immunoreactivity for endocrine secretory products was rarely noted, and only in a minority cell population (serotonin in two of ten). The majority of the tumors exhibited immunoreactivity for low molecular weight keratin (AE1/AE3 in eight of ten; CAM 5.2 in seven of nine), and three of ten tumors focally expressed high molecular weight keratin. Among the markers of neuroendocrine differentiation, neurospecific enolase was more frequently expressed (ten of ten) than chromogranin (five of ten) or argyrophilia (three of ten). Carcinoembryonic antigen was present in eight of ten tumors. S100 protein was absent in all cases. In summary, poorly differentiated small-cell carcinoids of the lower female genital tract, similarly to other small-cell endocrine tumors, occasionally exhibit focal glandular and squamoid differentiation, and only relatively infrequently or focally express immunohistochemically detectable endocrine secretory products, chromogranin, and argyrophilia.
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PMID:Endocrine and tumor differentiation markers in poorly differentiated small-cell carcinoids of the cervix and vagina. 302 70

In 72 patients with end-stage renal failure and 70 healthy subjects, the influence of blockade of opioid receptors by naloxone on secretion of prolactin, lutropin (LH), follitropin (FSH), adrenocorticotropin (ACTH), somatotropin (HGH), insulin (IRI), glucagon (IR-G), parathyroid hormone (PTH) and calcitonin (CT) was studied. Administration of naloxone stimulated luliberin-induced LH and FSH secretion quantitatively equally in patients and controls. Blockade of opioid receptors was followed by a less marked suppression of chlorpromazine-induced prolactin secretion but by a higher response of hypoglycemia-induced ACTH secretion in uremic patients than in controls. In addition, a less marked suppressive effect of naloxone was noted on hypoglycemia-induced HGH secretion in chronic renal failure as compared with controls. Blockade of opioid receptors improved significantly glucose tolerance and glucose-induced insulin secretion in uremic patients and suppressed nearly completely glucagon secretion response during the second phase of a glucose tolerance test. Finally, administration of naloxone was followed by a blunted response of Ca-induced CT secretion and suppression of PTH. Data presented in this paper suggest the existence of hyperendorphinism in end-stage renal failure.
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PMID:Effects of naloxone administration on endocrine abnormalities in chronic renal failure. 303 7


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