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)

Pituitary sections from 15 to 21 day-old rat foetuses have been studied with the immunofluorescence technique, using antibodies anti alpha-MSH, anti beta-MSH and anti beta (1-24) ACTH. The first ACTH cells appear on day 17 of pregnancy in the pars distalis of the hypophysis and only on day 18 in the pars intermedia. beta-msh cells have been observed on day 16 in the pars anterior and on day 17 in the pars intermedia, while alpha-MSH cells appear only on day 18 and exclusively in the pars intermedia. The cytodifferentiation of the beta-MSH and ACTH cells occurs in the pars intermedia with about a 24 hours delay in comparison to that of the pars distalis. The first revealed cells are always located in the posterior half of the pituitary gland. The corticostimulating activity of the hypophysis has been tested with the fluorescence intensity of the corticotrophs, the adrenal weight, the adrenal content in corticosterone and the plasma corticosterone level. The fluorescence of the corticotrophs increases on day 18, shows a maximum on day 19 and decreases until term. The adrenal weight rises regularly between day 16 to day 20, thereafer the increase subsides. Adrenal and plasma corticosterone concentrations reach a peak on day 19 of pregnancy. These data suggest that hypophyseal corticostimulating activity is very high between days 18 and 19 and decreases between days 19 and 21.
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PMID:Ontogenesis of the alpha-MSH, beta-MSH and ACTH cells in the foetal hypophysis of the rat. Correlation with the growth of the adrenals and adrenocortical activity. 16 96

In a group of 32 steroid-dependent asthmatic patients an attempt was made to replace steroid treatment with disodium cromoglycate (Lomudal). Withdrawal of steroids was accompanied by a transitory stage of combined corticotropin-Lomudal treatment for 6 to 8 mo. Pituitary-adrenal function was assessed by ACTH and Metopirone test. Before treatment an impairment of pituitary-adrenal function was found in most of our patients, although in 26 patients a normal increment of plasma cortisol was found after ACTH stimulation. At the end of the combined treatment, 17 patients are now on Lomudal with normal pituitary-adrenal function, 9 patients need small quantities of steroids occasionally, and 6 patients are steroid-dependent.
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PMID:Evaluation of pituitary-adrenal function in patients with chronic bronchial asthma following substitution of steroid treatment with disodium cromoglycate (Lomudal). 17 6

To investigate whether the hypothalamus is involved in the cytodifferentiation of the anterior pituitary gland, rat foetuses were encephalectomized in utero on day 16 of pregnancy. Pituitary sections from encephalectomized and normal littermate foetuses were studied on day 21 with the immunofluorescence technique using antibodies anti alpha-MSH, anti beta-MSH, anti alpha-(17-39) ACTH and anti beta-(1-24) ACTH. On day 16, only the anti beta-MSH revealed a few cells in the pars distalis but not in the pars intermedia. On the other hand, on day 21, the pituitary cells reacting with antibodies anti alpha-MSH, anti beta-MSH and anti alpha-(17-39) ACTH were as numerous in the encephalectomized foetuses as in the normal littermate foetuses. The cells revealed with the antibody anti beta-(1-24) ACTH were less numerous and less fluorescent in the pars distalis and intermedia of the hypophysis of the encephalectomized foetuses. On day 21, the adrenals of the encephalectomized foetuses were atrophied in comparison with those of the normal littermate foetuses but they were larger than on day 16. These data suggest that the cytodifferentiation of the corticotroph and melanotroph cells of the hypophysis occurs without the influence of the hypothalamus which is necessary for the normal release of ACTH.
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PMID:Hypothalamus and cytodifferentiation of the foetal pituitary gland. Study in vivo. 18 Nov 34

Pituitary control of pigmentation has known for more than 60 years. Since 1969, beta-melanocyte-stimulating hormone (beta-MSH) has been accepted as the main pituitary pigmentary hormone in man. Its "constant companionship" with adrenocorticotrophic hormone (ACTH) has also been repeatedly demonstrated. Current investigations challenge both of these concepts. Human beta-MSH immunoreactivity has been shown to be actually due to beta-lipotropic hormone (beta-LPH), a larger molecule that within itself contains the entire amino acid sequence of beta-MSH. Human beta-MSH does not exist in vivo; it is merely an extraction artifact formed by enzymatic degradation of beta-LPH. It would appear likely that beta-LPH, not beta-MSH, is the constant companion of ACTH.
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PMID:Pituitary pigmentary hormones. Relationship of melanocyte-stimulating hormone to lipotropic hormone. 21 Mar 1

Four cases of adrenoleukodystrophy (ALD) and one case of adrenomyeloneuropathy (AMN) have developed in a kindred over three generations demonstrating that AMN is a clinical variant of ALD. Pituitary-adrenal function studies were performed in 10 family members, including two affected males and four females identified as carriers of ALD/AMN. No pituitary-adrenal abnormality was found in the carriers. However, basal morning plasma adrenocorticotropic hormone (ACTH) levels were markedly elevated in the two males with ALD and AMN, despite the fact that they had no clinical signs of adrenal insufficiency and that morning plasma cortisol levels and their response to maximal exogenous ACTH stimulation appeared to be normal. In addition, the integrated 24-hour response to the administration were also subnormal in these two cases. Thus, people with ALD and AMN may have subclinical partial adrenocrotical insufficiency. No other endocrinologic dysfunction was identified.
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PMID:Adrenoleukodystrophy and adrenomyeloneuropathy associated with partial adrenal insufficiency in three generations of a kindred. 21 53

Differences in foetal and adult adrenal function may be due to qualitative as well as quantitative changes in the pituitary corticotrophic stimulus. Pituitary glands from adult and foetal sheep were freshly dissected and stored at -70 degrees C until extracted at pH 1.5. The extracts were subjected to chromatography on Sephadex G-100 superfine and fractions were assayed by multiple radioimmunoassays directed against the NH2- and CO2H-terminal sequences of ACTH and lipotrophin (LPH). Peaks corresponding to beta-melanocyte-stimulating hormone (beta-MSH), beta-LHP, gamma-LPH, beta-endorphin and ACTH were identified, with little or no evidence for the presence of alpha-MSH and corticotrophin-like intermediate lobe peptide. Three peaks of large molecular weight material, A. B and C, were identified and their relative proportions shown to be considerably greater in the foetus than in the adult. The immunoassay profile of peaks A and B suggested that they were 'stem hormones' which could give rise to a family of biologically active peptides. Since the 'family tree' which they engender varies according to the stage of development, it is proposed that the changes in the 'trophic family' may explain the different adrenal responses of the foetal and adult sheep.
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PMID:Adrenocorticotrophin-related peptides in adult and foetal sheep pituitary glands. 22 29

Groups of female rats were injected daily for 14 days with 10 mg of cortisone acetate subcutaneously, to study the mechanisms of glucocorticoid suppression on the hypothalamic-pituitary-adrenal axis. Pituitary adrenocorticotropic hormone (ACTH) content, plasma ACTH, adrenal venous corticosterone, adrenal weights, and the catabolic effects on body weight were studied simultaneously (under stressful and non-stressful conditions) before, during, and up to six weeks after cortisone. This study confirmed the results of other investigators that cortisone acetate caused catabolic weight loss and adrenal atrophy, but it was noted to persist up to six weeks after the injections. Glucocorticoid acetate was more effective in causing ACTH-axis suppression than succinate or phosphate preparations, and the effects were dose and time related. Significant depletion of pituitary ACTH content, suppression of plasma ACTH, and corticosterone secretion occurred five to seven days after beginning cortisone acetate (p=<0.001); it was continuous throughout the injection schedule (p=<0.001); it remained for two to four weeks after the cortisone was discontinued (p=<0.001). The animals showed minimum plasma ACTH responsiveness to severe acute stress during this two to four-week suppression phase, but rapid recovery occurred thereafter. Plasma ACTH was undetectable up to six weeks post-cortisone when the animals were not under stress. This may be related to residual cortisone acetate found at the injection sites, or to an altered or different ACTH-axis control mechanism. The sequence of events during recovery from cortisone suppression appeared to be (1) repletion of corticotrophin-releasing hormone (by inference), (2) repletion of pituitary ACTH content, (3) secretion of plasma ACTH, (4) reversal of adrenal atrophy, and (5) subsequent secretion of corticosterone.
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PMID:Suppression of the hypothalamic-pituitary-adrenal axis after subcutaneous cortisone acetate administration in rats. 22 95

The effects of beclomethasone, dipropionate aerosol (DBA) (400 microgram/day) on clinical course, pulmonary function, and pituitary-adrenal function was studied in 34 steroid-dependent asthmatic children. Asthma severity was assessed by daily symptom and medication scores, peak flow measured three times a day, and weekly spirometry. Pituitary-adrenal function was evaluated by diurnal cortisol levels, cortisol responses to intravenous (IV) corticotropin (ACTH), and steroid responses to IV metyrapone. After 12 weeks of BDA therapy, 30 of 34 patients no longer required prednisone. Mean weekly symptom and medication scores and the number of attacks decreased significantly (P less than .01)). A significant improvement was demonstrated in the patients' peak flow (P less than .01), forced expiratory volume in one second, and maximum midexpiratory flow rates (P less than .01). Thirty of the 34 patients initially had abnormal metyrapone responses, 28 had abnormal diurnal cortisol levels, whereas only 14 had abnormal IV ACTH response tests. Although significant improvement was noted in the mean metyrapone and diurnal cortisol tests, only partial recovery of pituitary-adrenal function was observed in 20 patients, complete recovery in 5, and no change in 9. BDA was found to be therapeutically superior to oral steroids in the group of steroid-dependent asthmatic children and produced no serious adverse effects.
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PMID:Treatment of chronic childhood asthma with beclomethasone dipropionate aerosols: II. Effect on pituitary-adrenal function after substitution for oral corticosteroids. 35 20

We have examined the hypothesis that MSH secretion in the rat is under a tonic inhibitory control by the central nervous system. Electrothermic lesions were made in the medio-basal hypothalamus (m.b.h.) which destroyed the hypothalamo-hypophyseal connexions. Plasma and pituitary alpha-MSH wwere measured using a sensitive and specific radioimmunoassay technique. Pituitary alpha-MSH content decreased to 17% of control levels 24 hr after the lesion and returned to normal by 7 days. Plasma alpha-MSH was maximally elevated 15 min after the lesion, and returned to normal by 2 hr. No further change over control levels was found for the remainder of the experiment (98 days). The similarity of the plasma alpha-MSH response after m.b.h. lesions to that found previously after administration of long acting dopamine receptor blocking drugs suggests that these lesions may interrupt impulse flow in dopaminergic tubero hypophyseal neurones which are thought to be important in the inhibitory control of MSH secretion in the rat. From our present results it seems that the rat pituitary, unlike that of lower vertebrates, is able to re-establish basal MSH secretion very quickly after disconnexion from central control.
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PMID:The effect of hypothalamic lesions on immuno-reactive alpha-melanocyte stimulating hormone secretion in the rat. 49 Mar 93

Rathke's pouch tissue, from rat embryos of 11-15 days' gestation, was microsurgically removed and transplanted into the hypothalamus of hypophysectomized adult females. The hosts were sacrificed 4 weeks later; brain and target organs were preserved for histological examination. Plasma samples were taken for the radioimmunoassay (RIA) of follicle stimulating hormone (FSH) and luteinizing hormone (LH). The implanted tissue invariably developed along certain lines. Undifferentiated primitive cells were found associated with nervous tissue, dense connective tissue, cartilage and glandular cells. In every age group, some implants became invasive, forming massive growths in the brain. These tumorous properties were principally associated (p less than 0.05) with tissue from 12-day embryos. Pituitary primordia from all ages demonstrated the ability to develop into functional adenohypophyseal tissue. Target organ stimulation indicated a secretion of corticotropin, thyrotropin and somatotropin. FSH and/or LH were detected by RIA in the plasma of 61% of the test animals. We suggest that this system offers unique opportunities for future investigations into the mechanisms that determine whether embryonic epithelial tissue will remain under normal growth control or will become tumorous or even cancerous.
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PMID:Development of Rathke's pouch tissue transplanted into adult hypophysectomized female rats. 122 58


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