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)

A simple and rapid assay for the quantitative determination of melanocyte-stimulating hormone (MSH) activity, using skin fragments of the lizard Anolis carolinensis in vitro, is described in detail. This assay, in which a quantal response (e.g. induction of a brownish-green colour) can be detected by visual observation, allows determination of MSH activity in up to 50 samples/day by one person, using the skin of one lizard. The mean dose found to induce this colour change was 0-15 ng synthetic alpha-MSH/ml (range 0-02-0-5 ng/ml). The assays shows high accuracy, reproducibility and specificity. Anterior and posterior lobe hormones as well as pituitary catecholamines do not interfere with the determination of pituitary MSH activitymthe method is compared with the assay using hypophysectomized frogs (Rana pipiens) in vivo. Determinations of MSH in pituitary extracts by both methods gave quantitatively similar results when determined with alpha-MSH as the reference substance. However, when beta-seryl MSH was used as a reference, the two assays gave different results for the MSH activity of the pituitary extractsmthis indicates that MSH from the rat pituitary gland has a biological activity similar to that of alpha-MSH rather than to that of beta-seryl MSH.
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PMID:Re-introduction and evaluation of an accurate, high capacity bioassay for melanocyte-stimulating hormone using the skin of Anolis carolinensis in vitro. 17 Mar 54

Serial sections from epoxy resin-embedded rat anterior pituitaries were sequentially immunostained for endorphin, [Met]enkephalin, and growth hormone, respectively. We found that [Met]enkephalin immunoreactivity was confined to the growth hormone producing cells. Corticotropin/endorphin cells in the anterior pituitary from both normal and adrenalectomized rats did not contain any [Met]enkephalin immunoreactivity. When anterior pituitary cells were maintained in monolayer culture for 10 days, [Met]enkephalin immunoreactivity was still located in the growth hormone-producing cells although the staining was weaker than in the somatotrophs in pituitary tissue fixed immediately after death of the animals. This suggested that somatotrophs synthesize [Met]enkephalin. However, this cannot be proved conclusively until biosynthesis experiments have been performed. The following conclusions were drawn from these findings. (i) Anterior pituitary [Met]enkephalin is not an extraction artifact derived from beta-endorphin with which it shares the NH2-terminal pentapeptide sequence. (ii) In the anterior pituitary, beta-endorphin is not the precursor to [Met]enkephalin. [Met]Enkephalin in somatotrophs may be of brain origin and in the somatotrophs may be bound to intracellllar receptors as has been shown for luteotropin releasing hormone in gonadotropic cells.
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PMID:Pituitary somatotrophs contain [Met]enkephalin-like immunoreactivity. 36 11

In separate experiments, nine (n = 20) and fifteen (n = 12) month old rats were treated with either 6% ethanol or 12% sucrose (to balance caloric intake) in the drinking water to examine the effect of chronic ethanol consumption on the hypothalamic-pituitary-adrenal axis of aged rats. Rats were maintained on these treatment regimens for thirty days and were killed by decapitation. Blood was collected and plasma concentrations of adrenocorticotropin (ACTH) and corticosterone were determined by radioimmunoassay. Adrenal glands were cleaned, quartered and used to test in vitro responsiveness to ACTH. Anterior pituitary glands from all 15 month old rats and one half of the nine month old rats were collected, frozen and extracted for measurement of tissue ACTH concentration. The remaining anterior pituitary glands from the nine month old rats were challenged with corticotropin releasing hormone (CRH) to test in vitro responsiveness. In nine month old rats, chronic ethanol consumption decreased plasma ACTH and corticosterone (P less than 0.05). Pituitary ACTH concentrations were unchanged in treated nine month old rats, but the amount of pituitary ACTH released in response to CRH was decreased (P less than 0.05) in rats consuming ethanol. In vitro responsiveness of the adrenal gland to ACTH in nine month old rats consuming ethanol was unchanged (P greater than 0.05). Plasma ACTH and corticosterone concentrations were also decreased in 15 month old rats chronically consuming ethanol (P less than 0.05). No differences were noted in responsiveness of the adrenal gland or in the amount of pituitary ACTH due to ethanol consumption in 15 month old rats (P greater than 0.05). The results of these experiments indicate that chronic ethanol consumption decreases hypothalamic-pituitary-adrenal function in aged rats.
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PMID:Chronic ethanol consumption depresses hypothalamic-pituitary-adrenal function in aged rats. 166 May 58

Prolactin (PRL) and alpha-melanocyte-stimulating hormone (alpha-MSH) are the only two pituitary hormones whose basal secretion is under tonic dopaminergic inhibition exerted by the hypothalamus. In the female rat, continuous exposure to estrogens is believed to depress hypothalamic dopaminergic activity and lead to the appearance of PRL-secreting pituitary adenomas during aging. Since there is no information about the impact of aging on circulating alpha-MSH levels, it was of interest to assess and compare the serum levels of PRL and alpha-MSH in male and female rats of different ages. Young (3-4 months) and old (24-25 months) male and female Sprague-Dawley rats as well as senescent (33-35 months) females were killed by decapitation between 10 AM and 1 PM, and pituitaries were immediately removed and dissected. Hormones were measured in unextracted trunk serum by radioimmunoassay. Serum PRL levels were (mean +/- SE), 18.4 +/- 2.0, 26.8 +/- 3.8, 19.8 +/- 2.5, 43.0 +/- 7.5, and 193.5 +/- 47.6 ng/ml for young and old males, and young, old, and senescent females, respectively. Serum alpha-MSH levels were 243.2 +/- 15.2, 252.9 +/- 24.8, 320.0 +/- 31.3, 234.7 +/- 19.1, and 374.0 +/- 29.7 pg/ml for young and old males, and young, old and senescent females, respectively. Anterior pituitary and neurointermediate lobe weights increased significantly with age in both sexes, although the change was particularly conspicuous in the females. We conclude that aging does not have a major impact on circulating alpha-MSH levels in rats and that melanotrophs probably have a greater ability than prolactotrophs to withstand age-associated alterations in central regulatory mechanisms.
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PMID:Differential effect of aging on serum levels of prolactin and alpha-melanotropin in rats. 184 77

The objectives of these studies were to examine the release of gonadotropin-releasing hormone (GnRH) and beta-endorphin-like activity (beta-EP) from macaque hypothalami, and the release of luteinizing hormone (LH) and GnRH-induced LH from macaque anterior pituitaries in response to neuropeptide Y (NPY) treatment. Anterior hypothalamic (AH) and mediobasal hypothalamic (MBH) blocks of tissues and the adenohypophysis were bisected along the midline into two equal-sized fragments. Fragments were superfused with medium for 3 h, followed by 3 h of either NPY (80 nM) or medium alone. In a separate experiment, adenohypophyseal (AP) fragments were superfused in accordance with the same protocol (3 h medium - 3 h NPY or medium) except that exogenous GnRH (352 nM) was added for 30 min at the beginning of hour 3 and again at the beginning of hour 6. Immunoactive GnRH, beta-EP, and LH levels were measured in superfusate samples (400 microliters) collected at 10-min intervals. GnRH levels rose within 20-30 min of initiation of NPY treatment, and elevated GnRH release was sustained for the duration of NPY exposure of both AH and MBH fragments from ovarian intact (INT) rhesus (Macaca mulatta: n = 8; p less than 0.05) or Japanese (Macaca fascicularis; n = 4; p less than 0.01) macaques. NPY treatment had no effect on either AH or MBH fragments isolated from ovariectomized (OVX) rhesus macaques (n = 4 for AH, and n = 5 for MBH). In AP fragments isolated from INT rhesus macaques (n = 8), NPY stimulated LH release within 1 h of treatment (p less than 0.05), whereas NPY had no effect on pituitaries from OVX animals (n = 4).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of neuropeptide Y on the in vitro release of gonadotropin-releasing hormone, luteinizing hormone, and beta-endorphin and pituitary responsiveness to gonadotropin-releasing hormone in female macaques. 204 72

Proopiomelanocortin is a polypeptide precursor molecule, the processing of which generates ACTH, beta-endorphin, the beta- and gamma-lipotropins, the joining peptide, and the NH2-terminal fragment. Anterior pituitary corticotrophs are the major site of proopiomelanocortin gene expression in man and the predominant, if not sole source of circulating ACTH. Recent data have established that proopiomelanocortin gene expression also occurs in various normal nonpituitary tissues, one of the best studied being the testis. In this latter organ the dominant gene products are short transcripts of approximately 800 nucleotides, which lack the first two exons of the gene and cannot encode a complete proopiomelanocortin molecule. In this report we show that the mode of proopiomelanocortin gene expression is occasionally modified in human Leydig cell tumors: a 1,200-nucleotide mRNA species identical to that in the pituitary is produced. It results from the usual (pituitary) start site of transcription and thus can encode the complete proopiomelanocortin molecule. In two out of six tumors, large amounts of the 1,200-nucleotide transcript led to a dramatic increase of approximately 1,000-fold in proopiomelanocortin peptide concentrations as compared with the normal and peritumoral testis. Proopiomelanocortin processing in these tumors generates various peptide fragments including ACTH. These results may help to understand the mechanism of proopiomelanocortin expression in nonpituitary tumors and have implications for the more general phenomenon of ectopic hormone secretion.
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PMID:Pituitary-like proopiomelanocortin transcripts in human Leydig cell tumors. 239 36

We investigated the effects of metabolites of arachidonic acid on the release of beta-endorphin-like immunoreactivity (beta-end-IR) from rat anterior pituitary cells. Anterior pituitary cells from female rats cultured with arachidonic acid released beta-end-IR in a dose- and time-dependent manner. To determine which metabolites of arachidonic acid stimulated the release of beta-end-IR, we examined the effects of an inhibitor of the cyclooxygenase, indomethacin, and an inhibitor of the 5-lipoxygenase, 2,3,5-trimethyl-6-(12-hydroxy-5,10-dodecadiynyl)-1,4-benzoquinone (AA-861). beta-end-IR release from pituitary cells induced by arachidonic acid was inhibited about 37% by AA-861, but was not affected by indomethacin. Other lipoxygenase inhibitors (eicosatetraynoic and nordihydroguaiaretic acid) also reduced the release of beta-end-IR induced by arachidonic acid. The effects of the 5-lipoxygenase products 5-hydroxy-6,8,11,14-eicosatetraenoic acid (5-HETE) and leukotrienes (LTA4, B4, C4, and D4) on the release of beta-end-IR from rat pituitary cells were also examined. 5-HETE (1-50 microM) elicited a dose-dependent release of beta-end-IR from cultured pituitary cells, and 50 microM 5-HETE induced beta-endorphin release time dependently. LTA4 and LTB4 also significantly stimulated the release of beta-end-IR, but LTC4 and LTD4 had no effect. Other lipoxygenase products (12-hydroxy-5,8,10,14-eicosatetraenoic acid, 12-HETE; 15-hydroxy-5,8,10,14-eicosatetraenoic acid, 15-HETE) were also secretagogues at concentrations of above 1 microM.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of release of beta-endorphin from rat pituitary cells. Role of lipoxygenase products of arachidonic acid. 252 76

Cushing's syndrome represents a constellation of symptoms of various origins. In most patients, detailed endocrinologic and radiologic testing will differentiate between Cushing's disease, adrenal adenoma, adrenal carcinoma, primary bilateral nodular hyperplasia, and ectopic corticotropin-producing tumors. Although adrenal surgery affords rapid and reliable remission in patients with Cushing's syndrome, it is associated with significant morbidity and mortality. Complications can be minimized by careful perioperative preparation. The indications for adrenal surgery for Cushing's disease have been altered radically by the success and low morbidity of transsphenoidal surgery. Total adrenalectomy is indicated in patients with bilateral nodular hyperplasia and should be considered for adults who have failed selective pituitary adenectomy or hypophysectomy and in whom ectopic corticotropin secretion has been unequivocally ruled out. At the Lahey Clinic, total adrenalectomy is performed through an anterior abdominal incision. Anterior approaches are especially indicated in those patients who require abdominal exploration for other intra-abdominal pathologic conditions that require surgery. Total adrenalectomy is indicated in the very rare patient who has Cushing's syndrome caused by ectopic corticotropin production when the patient is severely ill, a primary tumor is not found, and medical therapy fails or is poorly tolerated. Small adrenal tumors are best approached through a flank incision. Larger potentially malignant tumors should be approached through a thoracoabdominal incision.
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PMID:Surgical management of Cushing's syndrome. 266 80

In order to investigate the role of N-terminal proopiomelanocortin (N-POMC) in adrenal regeneration after bilateral adrenal enucleation (hereafter referred to as enucleation) rats 13 days after enucleation were injected (200 microliters s.c. plus 200 microliters i.p.) at 08.00 and 20.00 h with normal rabbit serum (NRS), an ACTH antiserum or an N-POMC antiserum. On the next day the animals were injected with colchicine, killed and mitotic figures in adrenal histological sections counted. The same treatment was given to rats 20 days after enucleation. Only the N-POMC antiserum significantly diminished adrenal mitotic activity 14 and 21 days after enucleation (P less than 0.01 and 0.05 respectively) when compared with NRS-treated enucleated rats, whereas plasma corticosterone levels in rats 14 days after enucleation were significantly (P less than 0.005) decreased only by treatment with ACTH antiserum. To determine whether the mitogenic N-POMC peptides involved in adrenal regeneration originated from the pituitary intermediate lobe, 0.9% (w/v) NaCl or ergocryptine (10 mg/kg body weight) was administered s.c. twice daily to rats between 7 and 13 days after enucleation. On day 14, adrenal mitotic activity and plasma levels of ACTH and N-POMC were not significantly different between ergocryptine and saline-treated enucleated rats, whereas alpha-MSH levels in ergocryptine-treated enucleated rats were significantly (P less than 0.02) decreased. Increases in N-POMC content of the pituitary lobe accompanied those of ACTH in animals 7, 10, 14 and 21 days after enucleation (P less than 0.01 compared with sham-treatment). Anterior lobes from rats 10 days after enucleation or from adrenalectomized rats showed raised ACTH and N-POMC levels compared with sham-treated animals, whereas alpha-MSH content in the anterior lobe of enucleated rats was significantly (P less than 0.005) decreased. Adrenalectomized animals had raised (P less than 0.005) amounts of alpha-MSH compared with sham-treated animals. Plasma levels of ACTH and N-POMC were significantly (P less than 0.01) raised in rats 10 days after enucleation or in adrenalectomized rats compared with those in sham-treated animals, whereas alpha-MSH levels were raised (P less than 0.005) only in adrenalectomized rats. Sephadex G-75 chromatography of anterior lobe extracts obtained 10 days after surgery from sham-treated, enucleated and adrenalectomized rats was performed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Adrenal regeneration in the rat is mediated by mitogenic N-terminal pro-opiomelanocortin peptides generated by changes in precursor processing in the anterior pituitary. 283 2

Anterior pituitary corticotropes represent only 9-10% of the mixed pituitary cell population. However, their small size precludes their enrichment because they cannot be separated from the more abundant PRL and GH cells. They can be induced to enlarge by adrenalectomy, and this report describes the separation of larger CRH-responsive corticotropes from a subpopulation of small pituitary cells. The separation was done by counterflow centrifugation in an elutriator containing the Sanderson chamber which was designed to separate small cells under 15 micron in diameter. The corticotropes were initially eluted at flow rates under 30 ml/min along with other cells less than 12.5 micron in diameter. They were then stimulated for 2-4 h with 0.5 nM CRH and reeluted with the use of higher flow rates to separate the enlarged corticotropes from the unstimulated cells. Reelutriation of the entire pool of small cells produced an enrichment to 60% corticotropes in five separate experiments. However, when the pool was divided into smaller cells (eluted at 20 ml/min) and medium-sized cells (eluted at 30 ml/min), and the two pools were reeluted separately, the enrichment increased to over 90% corticotropes in eight separate experiments. These corticotrope populations remained enriched for up to 14 days in culture. They also secreted in a reverse hemolytic plaque assay that recognizes ACTH-(25-39). The dual labels for ACTH and beta-endorphin showed that 60% of the corticotropes stored both peptides, whereas 30% stored only ACTH, and 10% stored only beta-endorphin. No differences in storage patterns were seen when small and medium-sized corticotropes were compared. Thus, these studies present the first report of the production of an enriched fraction of CRH-responsive corticotropes by counterflow centrifugation and the first report of heterogeneous storage of ACTH and beta-endorphin. The use of enriched fractions facilitated the analysis of these heterogeneous storage patterns in over 8000 corticotropes.
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PMID:Enrichment of corticotropes by counterflow centrifugation. 284 89


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