Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diazepam-induced feeding in rats is antagonized not only by the opiate antagonist naloxone but also intraventricular administration of specific antisera to the endogenous opioid peptides met-enkephalin or beta-endorphin. Pituitary beta-endorphin is probably not implicated in the diazepam effect since blockade with the glucocorticoid dexamethasone of the release of beta-endorphin from the anterior pituitary does not modify the diazepam-induced feeding, which is however prevented by TRH, a suggested physiological antagonist of some of the effects of opioid peptides. The possible central participation of both beta-endorphin and met-enkephalin in the ingestive behavior induced by diazepam gives further support to the postulated physiological role of endogenous opioids in appetite regulation.
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PMID:Antagonism of diazepam-induced feeding in rats by antisera to opioid peptides. 609 Aug 35

Development of the DMBA-induced breast cancer in rats resulted in an increase of the thyrotropin, somatotropin and prolactin concentrations in blood plasma. Thyroliberin (TRH) stimulation of the thyrotropin secretion was decreased. Basal levels of the corticotropin (ACTH) and lutropin (LH) as well as of the luliberin (LRH) stimulation of the LH secretion were not changed. Concentrations of estradiol, corticosterone and insulin enhanced, those of testosterone, progesterone and thyroxine lowered. Out of two calcitropic hormones, RTH and CT, the secretion of the latter increased.
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PMID:[Plasma hormone levels in rats with DMBA-induced mammary tumors]. 609 41

Several peptides are now known to affect thermoregulation. These include beta-endorphin, bombesin, MIF-I, alpha-MSH, neurotensin, TRH, and DSIP. Some of these have been found to interact with the thermal effects of d-amphetamine, a drug with well established actions on thermoregulation. The effects of morphine on body temperature provide some notable comparisons with beta-endorphin, as do the similarities between the effects of naloxone and MIF-I. In general, it seems that two of the major variables which interact and modify the thermal effects of peptides are ambient temperature and route of administration.
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PMID:Peptides and thermoregulation. 611 Jan 98

[125I]Iodo-Tyr1-somatostatin (SRIF) binds with high affinity to one class of sites in the rat anterior pituitary with a KD of 0.91 +/- 0.22 nM and a receptor concentration of 104.4 +/- 1.9 fmol/mg protein. This binding is saturable with respect to tissue concentration and is time-, temperature-, pH-, and calcium-dependent. It is also reversible as a function of time. The rates of association and dissociation were calculated to be 5.98 X 10(7) M-1 min-1 and 0.578 min-1, respectively. Binding of [125I]iodo-Tyr1-SRIF is not inhibited by morphine, beta-endorphin, [D-Ala2]Met-enkephalin, LHRH, TRH, histidylproline diketopiperazine, neurotensin, substance P, bombesin or vasoactive intestinal peptide. In contrast SRIF, [Tyr1]SRIF, and [D-Trp8,D-Cys14]SRIF displace [125I]iodo-Tyr1-SRIF binding with Ki values 0.10 +/- 0.05, 0.46 +/- 0.18, 0.05 +/- 0.01 nM, respectively. The constants of inhibition of a series of alanine monosubstituted analogs of SRIF are correlated (r = 0.89) with their biological potency on GH secretion. Furthermore, postnatal development patterns of [125I]iodo-Tyr1-SRIF binding sites follow the ability of SRIF to inhibit GH release. Thus, [125I]iodo-Tyr1-SRIF binding to adenohypophyseal membranes seems to reflect interaction with SRIF receptors on adenohypophyseal cells. Since biological effects of the peptide have been reported on GH, thyrotropin-stimulating hormone, and PRL secretion, further studies are required to determine the cell types upon which this binding occurs.
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PMID:Somatostatin receptors on rat anterior pituitary membranes. 612 57

The effect of VIP on prolactin secretion from incubated rat hemipituitaries was characterized. Under these conditions, the secretion of GH, LH, FSH, ACTH was not affected, indicating that the effect of VIP is hormone specific. The stimulation of prolactin was dose-dependent, with an apparent affinity of VIP of 10.9 +/- 3.1 nM and a maximal stimulation of 57.7 +/- 4.2%. Secretin, a structurally related peptide, was also active at higher concentrations, whereas another partial analogue, glucagon, was ineffective. Furthermore, VIP does not act through pituitary DA receptors since alpha-flupentixol, a potent dopaminergic antagonist, does not block the stimulation of prolactin secretion by VIP. In addition, stimulation by VIP and TRH was additive. Naloxone and met-enkephalin were ineffective on the VIP effect on prolactin release. In contrast, SRIF seems to inhibit the VIP stimulation of prolactin release. Our data suggest that VIP, which was found in the hypothalamo-hypophyseal blood at concentrations of the same order of magnitude as that found to stimulate PRL in vitro, could be a physiological PRF.
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PMID:[PRF activity of VIP in vitro (author's transl)]. 612 34

The tetrapeptide Tyr-Pro-Leu-Gly-NH2 (Tyr-MIFI) has been recently characterized in the hypothalamus and pineal of the rat. Since the concentration of Tyr-MIFI in the brain is increased by pinealectomy and is higher when the animals are in the dark, the possibility that Tyr-MIFI could be a physiological regulator of melanotropin secretion has been investigated. For this study a well-defined perifusion model has been applied, using whole neurointermediate lobes from male frogs (Rana ridibunda Pallas) or male Wistar rats. The amount of alpha-MSH released in the effluent perifusate was measured by means of a sensitive and specific radioimmunoassay method. For concentrations ranging from 10(-10) to 10(-6) M, Tyr-MIFI did not significantly alter the spontaneous release of alpha-MSH in the frog nor did it alter the release of alpha-MSH in the rat. Since it has been recently demonstrated that the tripeptide pGlu-His-Pro-NH2 (mammalian TRH) is a specific MSH-releasing factor in the frog, the possibility that Tyr-MIFI could modulate the response of the intermediate lobe of the frog to TRH has also been investigated. No alteration of TRH-induced alpha-MSH release was observed in the presence of a 100-fold excess of Tyr-MIFI. In addition, Tyr-MIFI was found to be unable to lighten the skin of the frog (Rana pipiens) when applied directly to the pituitary of the darkened animals. Thus these results definitively rule out the possibility that Tyr-MIFI is the melanotropin-release inhibiting factor in the frog or rat.
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PMID:Effect of Tyr-Pro-Leu-Gly-NH2 on melanotropin-stimulating hormone release in the frog and rat. 613 95

An intracisternal injection of somatostatin-28 produced hyperthermia in rats at cold, thermoneutral, warm ambient temperatures. The hyperthermic response to somatostatin-28 was not prevented by pretreatment of rats with the following agents: alpha-methylparatyrosine, phenoxybenzamine, propranolol, sulpiride, atropine, methysergide or naloxone. Somatostatin-28 prevented hypothermia induced by bombesin and gamma-MSH when it was administered simultaneously, but it left the hyperthermic response to TRH intact. The results indicate that somatostatin-28 produces hyperthermia by elevating a "set point" or regulated level of temperature. Under the conditions tested, the hyperthermic response to somatostatin-28 does not appear to be dependent on muscarinic cholinergic, serotonergic, alpha- or beta-adrenergic, dopaminergic or endogenous opiate system.
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PMID:Hyperthermic action of somatostatin-28. 613 57

Because hypothalamic and extrahypothalamic levels of thyrotropin-releasing hormone immunoreactivity (TRH-IR) undergo profound changes during the prenatal and early postnatal period in rats, similar effects with advanced aging were anticipated. For this reason we measured hypothalamic and reproductive tissue levels of TRH-IR, hypothalamic levels of somatostatin (SRIF), and beta-endorphin (EP), serum levels of prolactin (Prl), growth hormone (GH), thyrotropin (TSH), and thyroxine (T4) in young, sexually mature and 24-28 month-old male Long-Evans and Sprague-Dawley rats. Hypothalamic and prostatic levels of TRH-IR were consistently reduced as were the levels of T4 in old rats compared to young controls. Aging did not change the ratio of TRH to the major TRH-like peptide in prostates, as determined by high pressure liquid chromatography (HPLC) or the levels of hypothalamic SRIF and EP. All of the hypothalamic TRH-IR in both old and young male rats consisted of TRH by HPLC. Falling hypothalamic TRH levels and TRH secretory capacity may play a role in the blunted TSH response to cold stress in old rats.
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PMID:Thyrotropin-releasing hormone levels decrease in hypothalamus of aging rats. 615 Nov 24

Neuropeptides are sufficiently stable to allow valid radioimmunoassay of peptide concentrations in post-mortem human nervous tissue and in human cerebrospinal fluid. Studies have now documented abnormalities of peptide concentrations in degenerative diseases of the brain. Somatostatin concentration is reduced in the hippocampus and neocortex of patients dying with Alzheimer's type dementia. In Huntington's disease, there are reduced concentrations of substance P, met-enkephalin and cholecystokinin in the basal ganglia; in contrast the concentrations of somatostatin and TRH are increased. Immunocytochemical and experimental lesion studies are underway in an attempt to localize the peptide-containing cells affected by these disorders; and the potential role of alterations in neuropeptide function in the pathogenesis, clinical manifestations and therapy of these illnesses is of great interest. Although alterations of CSF peptide concentrations have been reported in a variety of human diseases, interpretation of these results requires knowledge of the origin and disposition of CSF peptides. Future research into the pathology of peptidergic systems will depend on the development of specific peptide antagonists to probe dynamic aspects of peptide function and on the application of the tools of molecular biology, such as specific mRNA assays, to human material.
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PMID:Implications of neuropeptides in neurological diseases. 620 11

To elucidate the regulation of secretion of beta-endorphin in Nelson's syndrome, both ACTH and beta-endorphin were measured using RIA. We found that beta-endorphin and ACTH were secreted concomitantly in responses to the administration of lysine-8-vasopressin and TRH. Conversely, the administration of somatostatin to this patient reduced the secretion of both beta-endorphin and ACTH. Thus, beta-endorphin is probably secreted cooredinately with ACTH in patients with Nelson's syndrome.
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PMID:Plasma beta-endorphin responses to somatostatin, thyrotropin-releasing hormone, or vasopressin in Nelson's syndrome. 624 30


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