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 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

Systematic pituitary evaluation was performed in four patients suspected of having Sheehan's syndrome. A sequential pituitary stimulation test, consisting of insulin-induced hypoglycemia followed by stimulation of gonadotropin-(GnRH) and thyroid-releasing hormone (TRH), a metyrapone test, and adrenocorticotropic hormone (ACTH) stimulation test, was performed. All four patients failed to develop a normal increase in serum growth hormone, cortisol, and prolactin (PRL) following insulin-induced hypoglycemia. All patients demonstrated a blunted PRL, follicle-stimulating hormone, and luteinizing hormone response to the combination of GnRH and TRH. Although thyroid stimulating hormone (TSH) response was impaired in all patients, two patients had normal T3 resin uptake and thyroxine, demonstrating minimal TSH reserve maintaining normal baseline free thyroxine index. Metyrapone administration was followed by no increase in 11-deoxycortisol or 17-ketogenic steroids, thereby adding no additional information to the hypoglycemia stimulation. ACTH infusion revealed normal adrenal cortisol response. In conclusion, in patients with suspected postpartum hypopituitarism, a complete pituitary function investigation can be done in a short time by using the described pituitary sequential stimulation test.
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PMID:Diagnosis of Sheehan's syndrome using a sequential pituitary stimulation test. 21 51

Regulation of corticotropin-releasing hormone (CRH) gene expression in vivo was assessed via in situ hybridization histochemistry, using probes directed against an intronic sequence of the CRH gene. Initial characterization of the CRH intron (CRHin) probe revealed specific localization of signal to the nuclear compartment of neurons in the medial parvocellular paraventricular hypothalamus, which are known to produce CRH peptide and mRNA. Abundance of CRHin signal was low, commensurate with a low resting pool of CRH heteronuclear RNA (hnRNA), representing CRH primary transcript. Regulation of CRH hnRNA levels was assessed after acute glucocorticoid synthesis blockade by injection of metyrapone. Metyrapone inhibits the conversion of 11-deoxycorticosterone to corticosterone, thereby rapidly depleting glucocorticoids and serving as a discrete stimulus for hypothalamo-pituitary-adreno-cortical activation. Plasma hormone measurements verified the efficacy of treatment, as metyrapone-treated rats showed extremely low basal corticosterone levels at all postinjection time points, while exhibiting progressive increases in plasma ACTH release over the 60-min postinjection period. CRH hnRNA levels were markedly increased 15-30 min after metyrapone injection, consistent with a rapid induction of CRH gene transcription in response to the stimulatory event. CRH mRNA, on the other hand, did not exceed control levels until 60 min post metyrapone, illustrative of a temporal lag between transcriptional changes and detectable changes in mRNA pools. Additional sections from metyrapone-and vehicle-treated rats were hybridized with probes complementary to mRNA encoding the immediate-early gene c-fos. c-fos was not present under unstimulated conditions yet was rapidly induced upon metyrapone treatment or vehicle injection (15 min).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Rapid regulation of corticotropin-releasing hormone gene transcription in vivo. 132 19

During long-term interferon alpha-2b (IFN) therapy of Philadelphia chromosome-positive chronic myelogenous leukemia (CML) patients, short-term effects of tumor necrosis factor alpha (TNF) on peripheral leukocyte counts, as well as cortisol and corticotropin (ACTH) release were studied. TNF (40-160 micrograms/m2) was given as a 2-h infusion on 5 consecutive days every 3 weeks, in addition to s.c. daily IFN injections (4 mio U/m2), to four (two male/two female) patients, who had been treated for more than 8 months with IFN and additionally for 0-7 months with TNF. Leukocyte counts, cortisol, and ACTH were determined at 30-min intervals between 4 p.m. and midnight. Profiles were determined the day before and on day 1 of TNF therapy. Leukocyte numbers decreased 30 min after start of TNF administration and increased 30-60 min later with a rebound until the next TNF application. The increase of leukocyte counts was due mostly to neutrophil granulocytes. ACTH levels increased 30 min, cortisol 60 min, and leukocyte counts 90 min after start of TNF infusion. Metopirone, an inhibitor of cortisol synthesis given to one patient, suppressed the TNF-induced stimulation of cortisol secretion and subsequent increase of leukocyte counts, while ACTH blood levels were enhanced. It was concluded that leukocyte count increases after TNF/IFN administration might be related to TNF-evoked cortisol secretion.
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PMID:Relation between leukocyte counts and cortisol secretion in CML patients undergoing combined TNF alpha/IFN alpha therapy. 132 78

The iron-containing protein cytochrome P-450 is present in high concentration in the adrenal cortex and is involved in the synthesis of corticosterone. This study was designed to determine the cortisol response to adrenocorticotropin (ACTH) in patients with severe iron deficiency. Eleven patients with iron deficiency and 15 normal controls were studied. Fasting blood samples were taken from all the subjects before and 30, 60 and 120 min after infusion of 25 units of ACTH for plasma cortisol determination. Six patients had blood samples collected at night, too. The same test was performed in 6 patients with iron deficiency, 7 days after therapy with 800 mg of ferrous sulfate. No significant differences were observed between patients and controls for the baseline cortisol values. The cortisol secretion and the increment at 30, 60 and 120 min after ACTH infusion were significantly lower in patients than in controls, either before or after ferrous sulfate therapy. There were no significant differences between baseline and stimulated cortisol values in patients before and after 7 days of ferrous sulfate therapy. There was no change in cortisol secretion rhythm in patients with iron deficiency (cortisol level at night = 5.1 +/- 4.3 micrograms/dl). In conclusion, the results of the present study showed that, in patients with severe iron deficiency, the cortisol secretion after ACTH stimulation was decreased.
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PMID:Reduced cortisol secretion in patients with iron deficiency. 165 78

The role of endogenous pyrogens induced by gram-positive bacterial pyrogens is not known. Intravenous alpha-MSH (2.5 micrograms) significantly reduced only the first phase of the biphasic thermal response to IV S. aureus cell walls (5 x 10(7)). Intracerebroventricular alpha-MSH (200 ng) had no effect on the fever response. The fall in serum iron concentration was significantly attenuated by the IV alpha-MSH but was not affected by the ICV alpha-MSH. Intravenous alpha-MSH had no effect on fever or the serum iron response caused by muramyl dipeptide (MDP). We conclude that the first phase of the thermal response to S. aureus cell walls is mediated by an endogenous pyrogen (EP) and the second phase of the response by a mechanism not involving EP, but possibly a muramyl peptide.
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PMID:The effect of alpha-MSH on fever caused by Staphylococcus aureus cell walls in rabbits. 166 87

Heavy metals including mercury, cadmium, cobalt, and copper (100 microM) exerted an adverse effect on the viability of isolated rat adrenal capsular (zona glomerulosa), adrenal decapsular (fasciculata and reticularis), and Leydig cells of the testis, with mercury being the most potent. Due to the decreased cell viability there was a parallel reduction in corticotropin-stimulated corticosterone production by adrenal decapsular cells and luteinizing hormone-stimulated testosterone production by Leydig cells. The results indicated a direct toxic action of these heavy metals on steroid-producing cells in the adrenal gland and the testis. Other metals tested, including lead, zinc, aluminum, chromium, iron, nickel, and lithium, did not exert any deleterious effect on cell viability or hormone-induced steroidogenesis in adrenal and Leydig cells when tested up to a concentration of 100 microM.
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PMID:Toxic effect of heavy metals on cells isolated from the rat adrenal and testis. 215 92

The aim of this study was to evaluate beta-endorphin, ACTH, and cortisol plasma levels during metyrapone administration in man after chronic opioid receptor stimulation. Metyrapone (750 mg every 4 hr for 6 doses) was administered to ten male heroin addicts, who had been on a maintenance therapy with methadone for at least 6 months and to ten healthy sex- and age-matched volunteers. Before metyrapone administration the basal levels of cortisol and ACTH were significantly decreased in addicts as compared to normal controls, while plasma beta-endorphin was not different. The response of beta-endorphin and ACTH to metyrapone administration was significantly blunted in addicts (p less than 0.01). These results suggest that the chronic stimulation of opiate receptors can impair the function of the anterior pituitary gland.
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PMID:Metyrapone effects on beta-endorphin, ACTH and cortisol levels after chronic opiate receptor stimulation in man. 217 17

We have developed a "sandwich"-type immunoradiometric assay for corticotropin (ACTH), with a detection limit of 2 ng/L. Two antibodies are used: a mouse monoclonal antibody directed against ACTH[1-17] and labeled with 125I; and a purified polyclonal goat antibody directed against ACTH[34-39] and conjugated to biotin. We could separate 125I-labeled antibody bound to ACTH from 125I-labeled antibody not bound to ACTH by using an avidin-biotin bridge, with avidin bound to a polystyrene ball. This assay reacts with ACTH[1-39] but shows no reaction with ACTH fragments [1-24], [1-17], or [34-39], or with melanotropin, endorphins, or lipotropin. This assay is sensitive enough to detect ACTH in plasma of all normal adults. Concentrations measured in 94 adults between 0800 and 1000 hours were normally distributed on a log scale, with a mean of 19.5 ng/L and a 95% range of 7.1 to 53.8 ng/L. Dexamethasone given at 2300 hours to 14 adults suppressed ACTH to less than 4 ng/L in 13 of the subjects and to 8 ng/L in the 14th. Metyrapone given to 13 adults at 2300 hours increased ACTH to 245.3 ng/L (95% range, 90.1 to 667.7 ng/L). This assay accurately classified patients with disorders of the adrenal system.
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PMID:Immunoradiometric assay of corticotropin with use of avidin-biotin separation. 254 49

Brain and blood iron deficiency (ID) can be nutritionally induced. Significant behavioral and brain-biochemical changes are observed in rats rendered iron deficient, including complete reversal of the circadian cycles of motor activity, changes in thermoregulation and stereotyped behavior, and an increased pain threshold. The increase in pain threshold is affected by diurnal factors and peripheral treatment with beta-endorphin has a significant analgesic effect, implicating selective changes in the blood-brain barrier. These effects along with modifications in responses to dopaminergic drugs, interactions of ID with neuroleptic drugs, and modifications in behavior as a result of selective brain lesions, lead to two conclusions: this animal model is appropriate for human anemia and the best explanation for the variety of behavioral and brain biochemical changes in ID rats is that the principal effect of brain ID is a selective decrease in the functional level of the dopaminergic D2 system.
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PMID:Brain iron: a lesson from animal models. 257 May 24


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