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)

Corticotropin-releasing hormone (CRH), somatostatin (SOM), delta-sleep-inducing peptide (DSIP), neuropeptide Y (NPY), beta-endorphin (beta-END), and vasopressin (AVP), which are regarded as being involved in the HPA-regulation were investigated in lumbar CSF of 44 suicide attempters. The patients were diagnosed according to the DSM-III-R, and rated with the MADRS. The neuropeptides were compared with the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in CSF and with post-dexamethasone plasma cortisol. We found strong correlations between CRH and the peptides SOM and beta-END. The latter also correlated positively with SOM. There were no differences between men and women. Patients with major depressive disorders had significantly lower SOM, CRH, and DSIP than other patients. Both SOM and beta-END correlated negatively with post dexamethasone plasma cortisol in all patients. We found no significant relationships between neuropeptides and CSF 5-HIAA. Patients who had made previous suicide attempts had significantly lower CRH than those who had not. No other significant associations between neuropeptides and suicidal subgroups of patients appeared, and there was no indication of specific neuropeptide patterns in patients who later completed suicide. Intercorrelations of some neuropeptides and low SOM and DSIP in major depressed patients are findings in line with those by others.
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PMID:HPA-related CSF neuropeptides in suicide attempters. 137 70

The opioid peptides methionine enkephalin (M-ENK) and beta-endorphin (beta-END) (1 x 10(-5)-1 x 10(-11) mg/ml) were investigated for their effect on the PHA (1:500, 1:750 or 1:1000) induced proliferative response of old and young Wistar rat splenic lymphocytes in vitro. The different effects in young and old rats on proliferative response to PHA were determined. The results showed that MENK and beta-END significantly enhanced the proliferative response to PHA in young rats, while enhancement by M-ENK and beta-endorphin (PHA 1:750, 1:1000) was not observed in old rats. The PHA-induced proliferative response was 30%-40% lower in old rats than in young rats. Our results suggest an altered response to neuro-immunomodulation with age. The in vitro effect of ENKs on phagocytosis was also studied. The results indicated that LENK (10(-4)-10(-6) mg/ml) and MENK (10(-2)-10(-4) mg/ml) could stimulate the phagocytosis of peritoneal macrophages from Balb/c mice.
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PMID:[Ageing suppresses the enhancement of T cell mitogenesis by opioid peptides and enkephalins increase phagocytosis of murines macrophage]. 139 43

Central administration of neuropeptide-Y (NPY) inhibits pituitary LH release in ovariectomized rats and stimulates LH release in intact and ovariectomized rats pretreated with ovarian steroids. Although the precise neural mechanism of this dual effect of NPY is not known, experimental evidence suggests an underlying interaction between hypothalamic NPY and the inhibitory beta-endorphin (beta END) systems in the neuroendocrine regulation of pituitary LH release in the rat. The present study was undertaken to examine the morphological basis of the interaction between these two peptidergic systems in the hypothalamus. Sections of the mediobasal hypothalamus of colchicine-pretreated female rats were double immunostained for NPY and beta END and examined by light and electron microscopy. The light brown diaminobenzidine reaction was used to visualize beta END cells, while NPY neurons were labeled with a dark blue nickel ammonium sulfate-intensified diaminobenzidine reaction. Under the light microscope, a dense network of NPY-immunoreactive axons and axon terminals was observed in close apposition with beta END-immunoreactive neurons throughout the medial basal hypothalamus. Electron microscopic examination revealed that NPY-immunoreactive boutons formed axosomatic and axo-dendritic synaptic connections with beta END cells. A majority of these synaptic membrane specializations appeared asymmetrical [corrected]. In light of the previous evidence of excitatory and inhibitory effects on LH release and the existence of direct synaptic connections between NPY and LHRH neurons in the hypothalamus, the current results imply that the dual effects of NPY on LH secretion may involve modulation of LHRH secretion, both by the direct route and indirectly through the hypothalamic beta END system.
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PMID:Neuropeptide-Y innervation of beta-endorphin-containing cells in the rat mediobasal hypothalamus: a light and electron microscopic double immunostaining analysis. 142 43

Deficiency in the secretion of luteinizing hormone-releasing hormone (LHRH) from the median eminence (ME) is one of the factors limiting reinitiation of estrous cycles following parturition in cows. In previous studies, administration of naloxone, an opioid receptor antagonist, to postpartum cows increased LH secretion, suggesting that endogenous opioids inhibit the secretion of LHRH. This study employs quantitative light microscopy to describe morphological changes in the distribution of immunoreactive beta-endorphin (ir-beta-END) neurons in the hypothalamus of anestrous early postpartum (EPP, days 10-16, n = 5), midpostpartum (MPP, days 33-43, n = 4) and multiparous cycling cows (CYC, months 12-14, n = 4). Cryostat sections (60 microns) of perfusion-fixed ventral diencephalon and forebrain were immunostained with anti-beta-END serum via the biotin-avidin-peroxidase method or double stained sequentially with anti-LHRH serum, then anti-beta-END serum. In all cows, beta-END immunoreactive perikarya, mostly bipolar neurons, were located in the arcuate and periarcuate nucleus (ARC), with some perikarya in the ME. Within the ARC, the percentage area immunostained for ir-beta-END was greater (p < 0.01) for the CYC than EPP cows, with MPP intermediate but not significantly different from the other groups. Consistent for all cows, the percentage area of ir-beta-END in ventral ARC regions was greater (p < 0.05) than dorsal ARC regions. Fibers from these neurons coursed into the anterior hypothalamus, preoptic area and bed nucleus of stria terminalis. Ventrally projecting fibers entered the ME forming a densely staining band within the external layer.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Distribution of beta-endorphin immunoreactivity in the arcuate nucleus and median eminence of postpartum anestrus and luteal phase cows. 143 81

The effects of systemically administered clonidine on pituitary-adrenocortical axis in morphine-tolerant rats and after naloxone-induced withdrawal were examined. In naive animals, clonidine (0.5 and 1 mg/kg s.c.) significantly increased plasma beta-endorphin-like immunoreactivity (beta-END-LI) and cortisol levels. This effect was significantly reduced in morphine-tolerant animals. Naloxone treatment induced an increase of plasma beta-END-LI and cortisol levels in morphine-tolerant animals. The increase in cortisol level after withdrawal was significantly reduced by clonidine. These results are consistent with an interaction between alpha 2-adrenoceptors and opioid systems in the control of pituitary-adrenocortical axis during morphine tolerance and withdrawal.
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PMID:Effects of clonidine on pituitary-adrenocortical axis in morphine-tolerant rats and after naloxone-induced withdrawal. 157 97

Physiological and pathological evidence suggests that opioid peptides may play a role in glucose homeostasis. We measured plasma levels of beta-endorphin (beta-END) and met-enkephalin (met-ENK) in 22 type I diabetic patients and 15 healthy women (control group). No differences were observed in plasma beta-END levels, whereas plasma met-ENK levels were significantly higher (Student's t test, P less than .005) in diabetics than in controls before (68 +/- 3 pg/mL v 32 +/- 7 pg/mL) and 1 hour after, a standard meal and administration of insulin therapy (81 +/- 9 pg/mL v 32 +/- 7 pg/mL). This is the first report of met-ENK levels in insulin-dependent diabetes mellitus (IDDM), and an impaired feedback of insulin/met-ENK is suggested.
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PMID:Plasma met-enkephalin in type I diabetes. 158 23

In several diseases chronic pain is associated with long-lasting pathophysiological responses which differ strongly from those observed in acute situations. When persisting, acute pain often results in physical and psychological stress which may in turn aggravate the initial pathological state. In the present work we examined the secretory patterns of pituitary hormones related to acute stress (growth hormone (GH), prolactin (PRL) and beta-endorphin (beta-END)) in rats during the phase of Freund adjuvant-induced arthritis (AIA, a model used for chronic pain studies) when chronic pain is maximum (14 and 21 days, postinoculation (PI)). Using radio-immunoassay hormones were measured in plasma samples taken every 30 min for 7 h in free-moving rats 14 and 21 days after Freund adjuvant or vehicle injection and in control animals. The total amount of GH secretion was higher at 14 and 21 days PI in AIA rats as compared to vehicle-treated and control animals, and the pulsatility of GH secretory pattern was not modified by AIA. PRL and beta-END secretion were not significantly different in arthritic rats as compared to controls. These results show that GH, PRL and beta-END responses induced by acute stress are not observed during the AIA phase when chronic pain is maximum. Thus, in our experimental conditions, beta-END and PRL do not seem to be good plasma markers of chronic pain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic pain induces a paradoxical increase in growth hormone secretion without affecting other hormones related to acute stress in the rat. 159 79

Immunoreactive beta-endorphin (IR-beta END) is present in human endometrium. Several indirect lines of evidence suggest that endometrial beta END is under steroid hormone control, i.e. IR-beta END is detectable in the secretory, but not the proliferative, endometrium, and progesterone administration increases the concentration of IR-beta END in uterine secretions of ovariectomized gilts. To study the effect of steroid hormones on endometrial beta END, we first questioned whether Ishikawa human endometrial adenocarcinoma cells (which respond to steroid hormones) express the proopiomelanocortin (POMC) gene. Indeed, on Northern blot analysis, a RNA similar or identical in size to pituitary POMC mRNA was present in Ishikawa cell RNA extracts. IR-beta END was also present in Ishikawa cell extracts and culture medium, which coeluted with synthetic human beta END in a Sephadex G-50 column. Ishikawa cells released most of their IR-beta END into the culture medium. Estradiol decreased the release of IR-beta END from Ishikawa cells, an effect that was dependent upon dose and time. The maximal effect was observed after a 4-day exposure to 10 nM estradiol (44 +/- 6% of the control value; n = 6; P less than 0.001). This effect was almost completely counteracted by a 100-fold excess of the antiestrogen 4-hydroxytamoxifen. Progesterone and dihydrotestosterone did not have a statistically significant effect on IR-beta END release. Dexamethasone had effects similar to those of estradiol, i.e. decreased the release of IR-beta END in a time- and dose-dependent manner. The maximal effect was detected after a 4-day exposure to 10 nM dexamethasone (53 +/- 6% of the control value; n = 6; P less than 0.001). Interestingly, the antiprogestin-antiglucocorticoid RU486 exhibited agonistic properties, i.e. diminished the release of IR-beta END in a time- and dose-dependent fashion, possibly via the glucocorticoid receptor. Its maximal effect was reached after a 4-day exposure to 10 nM RU486 (55 +/- 6% of the control value; n = 6; P less than 0.001). In conclusion, our data demonstrate that the release of IR-beta END from Ishikawa cells in culture is inhibited by estradiol and dexamethasone, suggesting that endometrial beta END is under estrogen and glucocorticoid regulation, as is the case with hypothalamic and pituitary POMC-derived peptides. This is the first time that the in vitro release of a peripheral-extracranial POMC-derived peptide has been found to be under the direct control of estrogens and glucocorticoids.
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PMID:Steroid hormones regulate the release of immunoreactive beta-endorphin from the Ishikawa human endometrial cell line. 163 59

To study the role of corticotropin-releasing hormone (CRH) in the circadian rhythm of circulating corticotropin (ACTH), beta-endorphin (beta-END), corticosterone, and prolactin (PRL), we measured the effects of CRH immunoneutralization over a 24-hour period in chronically cannulated, conscious, freely moving, male Sprague-Dawley rats, maintained at a constant light-dark cycle. Blood samples were collected in the morning (08.00 h), at noon (12.00 h), and in the evening (18.00 h) on the day of treatment, and in the morning (08.00 h) of the next day. Hyperimmune rabbit serum raised against rat CRH (1.0 ml/rat, i.v.) or normal rabbit serum (NRS, 1.0 ml/rat, i.v.) was administered at 08.00 h, immediately after the first blood sample had been collected. CRH immunoneutralization caused no significant decreases in circulating immunoreactive ACTH, beta-END and corticosterone plasma levels at noon, but abolished the evening rises of these hormones. PRL levels were not significantly different between the groups at any time point measured. To compare the effects of CRH immunoneutralization to those of glucocorticoid negative feedback, we measured the effects of dexamethasone (0.5 mg/kg, i.v. at 08.00 h) on the above parameters. ACTH and beta-END concentrations were significantly decreased, and corticosterone and PRL levels were markedly suppressed after glucocorticoid administration both at 12.00 and 18.00 h. However, 24 h after the administration of dexamethasone, PRL concentrations were elevated despite persistently low corticosterone levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Circadian patterns of plasma immunoreactive corticotropin, beta-endorphin, corticosterone and prolactin after immunoneutralization of corticotropin-releasing hormone. 165 9

The fasting plasma levels of corticotropin-releasing hormone (CRH), delta sleep-inducing peptide (DSIP), beta-endorphin (beta-END), methionine-enkephalin (m-ENK), beta-lipotropin (beta-LPH), and alpha-melanocyte-stimulating hormone (alpha-MSH) were measured by radioimmunoassay in 22 stable patients with chronic renal failure on regular hemodialysis treatment and compared with those of 10 healthy controls. The plasma concentrations of DSIP, beta-END, m-ENK, beta-LPH, and alpha-MSH were increased. The plasma level of CRH was not different from that of the controls. The elevated plasma levels of endogenous opioid peptides and DSIP may contribute to the uremic syndrome, although this must be further elucidated.
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PMID:Elevated plasma levels of opioid peptides and delta sleep-inducing peptide but not of corticotropin-releasing hormone in patients receiving chronic hemodialysis. 166 74


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