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)

Cushing's disease developed in a 5-year-old girl with acute lymphoblastic leukemia 18 months after her last therapeutic exposure to adrenal glucocorticosteroids. Obesity, hyperpigmentation, striae, osteoporosis, and hirsutism were accompanied by elevated levels of plasma cortisol. These showed no diurnal fluctuation and they were not suppressed by dexamethasone. At autopsy, the adrenal glands were enlarged and the pituitary gland showed increased numbers of basophils of the adrenocorticotropic hormone (ACTH)/melanocyte-stimulating hormone secreting type. Leukemic infiltrates in brain tissue were prominent in the hypothalamus and in the limbic system. It is postulated that the destructive leukemic infiltrate of the limbic system removed a restraining influence on pituitary function, with basophilic hyperplasia, ACTH hypersecretion, adrenocortical hypertrophy, and clinical Cushing's disease the consequences.
Am J Dis Child 1978 Sep
PMID:Cushing's syndrome and acute lymphoblastic leukemia. 27 79

Tolerance to beta-endorphin developed acutely in cats if the administration of the peptide was repeated within the first 24 hr. The tolerance was reversed immediately by systemic administration of the serotonin precursor, 5-hydroxytryptophan. It was further shown that 5-hydroxytryptophan potentiates the analgesic effect of the subliminal dose of beta-endorphin.
Proc Natl Acad Sci U S A 1977 Sep
PMID:beta-Endorphin: development of tolerance and its reversal by 5-hydroxytryptophan in cats. 30 46

The effect of synthetic melanocyte-stimulating hormones (MSH) on urinary excretion of sodiu, potassium and water was studied in hamsters. Synthetic alpha-MSH and synthetic human beta-MSH showed a marked natriuretic and diuretic effect depending on the dosage of hormone. The natriuretic effect of both hormones was approximately equal and did not parallel the magnitude of the melanocyte-stimulating activity of the investigated peptides. Both peptides showed also a milder kaliuretic effect independent on their dose. The rise of the sodium/potassium index in urine was significant after both peptides. Bilateral adrenalectomy increased further the natriuresis induced by alpha-MSH, while it did not affect the effect o MSH on diuresis and kaliuresis. Changes in urinary excretion of sodium and potassium are considered to be consequence of direct renal action of MSH.
Endocrinol Exp 1979 Sep
PMID:Natriuretic and kaliuretic effect of melanocyte-stimulating hormones in hamsters. 31 65

Lutropin and human choriogonadotropin stimulated the endogenous chromatin-associated polymerase activity in purified chromatin prepared from nuclei of bovine corpus luteum. Chromatin was incubated in two different buffer systems: one that mainly supports the activity of polymerase I, another that supports the activity of polymerase II and is largely alpha-amanitin sensitive. The hormones lutropin and chorigonadotropin stimulated an increase in the rate of incorporation of [14C]ATP or [14C]UTP into RNA in both buffer systems. Follitropin, prolactin and beta-corticotropin had no stimulatory effect. Neither the alpha nor beta subunit of lutropin stimulated RNA synthesis. When premixed, the subunits rapidly formed the active molecule. A maximum response to RNA synthesis was achieved by a 10(-9) M concentration of human choriogonadotropin. Considerable activity was obtained at 10(-11) M human choriogonadotropin. There was no lutropin stimulation to RNA synthesis using calf thymus DNA and Escherichia coli RNA polymerase.
Biochim Biophys Acta 1977 Sep 06
PMID:Lutropin stimulation of RNA synthesis in corpus luteum chromatin. 32 86

Using an immunohistochemical technique at the electron microscopic level, it has been shown that alpha-MSH is localized within the small vesicles of a few cell bodies found in the arcuate nucleus and numerous nerve fibers widely distributed throughout the brain. These findings suggest that alpha-MSH could possibly be considered as a neurotransmitter.
Am J Anat 1977 Sep
PMID:Electron microscopic immunohistochemical localization of alpha-msh in the rat brain. 33 90

Immunocytochemistry was utilized to determine if pars tuberalis cells in the pituitary of the monkey (Macaca mulatta) have the potential to elaborate gonadotropic and thyrotropic hormones normally secreted by the pars distalis. A total of 7 males and females were studied. The hormones were localized by the peroxidase-antiperoxidase method of Sternberger, and utilized with antisera to the following human hormones: somatotropin, mammotropin, beta(1-24)-corticotropin, chorionic gonadotropin, and the beta-subunits of follicle stimulating hormone and thyrotropin. Many of the parenchymal cells in the pars tuberalis of the median eminence were composed of gonadotropic cells, probably containing luteinizing hormone and follicle stimulating hormone, and thyrotropic cells. Corticotropic and somatotropic cells were seen only rarely, and mammotropic cells were undetectable. The results indicate that the pars tuberalis is able to secrete luteinizing hormone, follicle stimulating hormone, and thyrotropin.
Biol Reprod 1977 Sep
PMID:The presence of gonadotropic and thyrotropic cells in the pituitary pars tuberalis of the monkey (Macaca mulatta). 40 48

With an antiserum against human beta-endorphin (beta-EP) crossreacting less than 2% with human beta-lipotropin (beta-LPH) by weight we have developed a radioimmunoassay that can detect 1 pg beta-EP in diluted raw plasma. In a.m. fasting plasma of 14 normal subjects beta-EP ranged from less than 5 to 45 pg/ml. beta-EP was elevated in untreated, but normal in successfully treated Cushing's disease; undetectable in a patient with adrenal adenoma; extremely high in Nelson's syndrome; and elevated in a patient with bronchogenic carcinoma before, but undetectable after tumor resection. In subjects with intact hypothalamic-pituitary-adrenal axis, beta-EP was undetectable after dexamethasone and increased after metyrapone administration and insulin-induced hypoglycemia. beta-EP concentration was considerably lower in serum than in simultaneously collected plasma, but increased in serum left unfrozen for several hours after clot removal. Thus, beta-EP behaves like a hormone responding to the same stimuli as ACTH and beta-LPH and blood appears to contain enzymes both generating and destroying immunoreactive beta-EP.
J Clin Endocrinol Metab 1979 Sep
PMID:Specific radioimmunoassay of human beta-endorphin in unextracted plasma. 46 83

Plasma beta-endorphin-like immunoreactivity was measured by a method that was equally sensitive to beta-endorphin and [Leu5]-beta-endorphin. Immunoreactivity in 98 schizophrenic patients did not differ greatly from that in 42 normal subjects. No immunoreactivity was detectable in dialyzates from first-time hemodialysis of eight nonpsychotic renal patients and nine schizophrenic patients. These results are not compatible with recent reports of extremely high concentrations of [Leu5]-beta-endorphin in hemodialyzates from schizophrenic patients.
Science 1979 Sep 14
PMID:Plasma beta-endorphin immunoreactivity in schizophrenia. 47 35

The cholinergic agonists, pilocarpine, physostigmine and nicotine, inhibited the prolactin release induced by morphine in male rats in vivo. Pilocarpine also inhibited the release of prolactin induced by beta-endorphin or metoclopramide without affecting the basal and haloperidol-stimulated serum prolactin levels. The inhibitory effect of pilocarpine on the morphine-stimulated release of prolactin was antagonized by concurrent administration of atropine but not by atropine methylnitrate or by mecamylamine, while the inhibition by nicotine was antagonized by mecanylamine but not by atropine. The stimulation of prolactin release by morphine and its reversal by pilocarpine were observed after the administration of haloperidol or alpha-methyltyrosine. These results suggest that the central cholinergic system exertes an inhibitory influence on the prolactin release induced by morphine or beta-endorphin and the cholinergic inhibition is not mediated via catecholaminergic neurons.
Naunyn Schmiedebergs Arch Pharmacol 1979 Sep
PMID:Inhibition by cholinergic agonists of the prolactin release induced by morphine. 50 52

1. A new line of cloned, differentiated rat hepatocytes (RL-PR-C) was evaluated for its usefulness as an in vitro system for studying the regulation of the insulin receptor. 2. Insulin rapidly reversibly and specifically bound to RL-PR-C hepatocytes. Binding of tracer 125I-labeled insulin, which was competitively inhibited by native insulin as well as by proinsulin and analogs of insulin and proinsulin in proportion to their biological activity, was not influenced by glucagon, corticotropin, or human growth hormone. Anti-insulin receptor serum from a patient with Acanthosis Nigricans Type B competed with 125I-labeled insulin for binding to cell surface sites. 3. Trypsinization destroyed insulin binding sites, but these were restored by incubation under growth conditions; a 75% restoration of binding sites was achieved by one cell population doubling. 4. RL-PR-C hepatocytes responded to insulin binding by an increase in glycogen synthesis from glucose. The insulin effect was maximal at 85 nM, but was detectable at lower, more physiological, concentrations. 5. Chronic exposure (for at least 3h) of hepatocytes to insulin (10(-10)--(10(-8) M) reduced by up to 60% the number of binding sites for insulin (down-regulation). Down-regulation was prevented by cycloheximide at concentration (10 micron) sufficient to inhibit markedly protein synthesis from tracer isoleucine. Recovery from down-regulation induced by native insulin at 10(-7 M or lower concentrations was complete by 18 h under growth conditions. 6. Although RL-PR-C hepatocytes spontaneously transform after about 90 population doublings, no significant differences between normal and transformed cells were observed in insulin binding characteristics and in interaction of cells with anti-insulin receptor serum. However, transformed cells exhibited a substantially reduced (maximum of 20%) down-regulation response to insulin. 7. RL-PR-C rat hepatocytes appear, for these reasons, to be a useful model system for studying the regulation of the insulin receptor.
Biochim Biophys Acta 1978 Sep 06
PMID:Hormone receptors. 7. Characteristics of insulin receptors in a new line of cloned neonatal rat hepatocytes. 56 93


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