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)

Utilizing push-pull perfusion, we examined secretory profiles of corticotropin releasing hormone (CRH) in the median eminence (ME) and of plasma adrenocorticotropin (ACTH) in freely moving male rats after intravenous bolus injection of recombinant human interleukin (IL)-1 alpha (1.0 microgram) and 1 beta (1.0 microgram). The ME was perfused with artificial cerebrospinal fluid between 11.00 and 14.00 h, and perfusates and blood samples were collected every 20 min. Administrations at 12.00 h of IL-1 alpha and 1 beta, but not vehicle only, resulted in significant increases in both the plasma ACTH and ME-CRH. The rise in ME-CRH clearly preceded the enhanced ACTH secretion. These in vivo data strongly suggest that IL-1 stimulates ACTH secretion, at least in part, by triggering hypothalamic CRH release. This is the first to characterize the temporal profile of CRH secretion in the ME after intravenous administration of IL-1 to freely moving rats.
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PMID:Evidence that intravenous administration of interleukin-1 stimulates corticotropin releasing hormone secretion in the median eminence of freely moving rats: estimation by push-pull perfusion. 166 17

The peripheral secretion of endogenous opioids was studied in 10 women with restrictive anorexia nervosa and 10 age- and sex-matched healthy controls. The circadian rhythm of beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH), and their responses to the administration of corticotropin releasing hormone (CRH, 1 micrograms/kg body weight, i.v.), clonidine (150 microgram, i.v.), domperidone (10 mg, i.v.), and 5-hydroxytryptophan (5-HTP, 200 mg, p.o.) were examined in patients and controls. The results revealed increased nocturnal secretion of beta-EP and diurnal-nocturnal secretion of beta-LPH with loss of circadian rhythmicity of both peptides, normal response to CRH stimulation, blunted response to clonidine and domperidine, and normal beta-EP and blunted beta-LPH response to 5-HTP stimulation. The data suggest a complex alteration of peripheral opioids and of central aminergic mechanisms that regulate proopiomelanocortin-derived peptide secretion and eating behavior.
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PMID:Peripheral opioid secretory pattern in anorexia nervosa. 166 17

Using in situ hybridization histochemistry, corticotropin-releasing hormone gene expression is first detectable in the parvocellular portion of the rat paraventricular nucleus on the 17th fetal day. The prevalence of messenger RNA for corticotropin releasing hormone decreases perinatally, specifically between the 19th and 21st fetal days. By the 4th postnatal day, CRH gene expression is similar to that of the adult rat. Somatostatin messenger-RNA is detectable on the 14th fetal day in the periventricular nucleus. No perinatal hiatus in somatostatin gene expression is evident.
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PMID:Ontogeny of corticotropin releasing hormone gene expression in rat hypothalamus--comparison with somatostatin. 168 45

In mouse, rat, and monkey, N-methyl-D,L-aspartic acid (NMDA) modulates gonadotropin releasing hormone (GnRH) release by an unknown mechanism. In previous studies we found that normal male mice consistently responded to NMDA administration with increased levels of plasma LH, as did most normal female mice and female hypogonadal mice with fetal preoptic area implants (HPG/POA). To investigate the mechanism of NMDA-induced GnRH release, immunocytochemistry of c-fos protein (FOS) was used for detection of neurons activated by NMDA administration. In both normal male and HPG/POA mice, FOS expression was unchanged in GnRH cells after NMDA administration. That neurosecretory cells can respond to NMDA was shown by the induction of FOS in many CRH (corticotropin-releasing hormone) cells in the paraventricular nucleus. Immunocytochemistry of beta-Endorphin, neuropeptide Y, tyrosine hydroxylase, an enzyme marker for catecholaminergic neurons, and glutamic acid decarboxylase, an enzyme marker for GABA neurons, was combined with that for FOS in normal male mice. Many noradrenergic (NA) neurons in the locus coeruleus (32-61%), and dopaminergic (DA) neurons in the mediobasal hypothalamus (15-31%) expressed FOS after NMDA administration while FOS was only rarely induced in neurons with the other neuromodulators tested. FOS was also induced in the locus coeruleus in male (43, 54%) and female (40, 55, 69%) HPG/POA mice. In contrast, few cells of the locus coeruleus expressed FOS in normal or HPG/POA mice after saline challenge. These results suggested that NMDA did not activate GnRH cells directly, but that NA neurons in the locus coeruleus were activated by NMDA and might be involved in stimulating GnRH release.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Norepinephrine neurons in mouse locus coeruleus express c-fos protein after N-methyl-D,L-aspartic acid (NMDA) treatment: relation to LH release. 168 42

Bilateral, selective, and simultaneous catheterization of the inferior petrosal sinus is not only a valuable tool in the differential diagnosis of Cushing's syndrome, but may also provide new insights into paracrine interactions at the pituitary level. We have investigated whether CRH (1 microgram/kg BW) has any effect on the release of PRL, GH, TSH, or the alpha-subunit of hCG during this procedure. Sixteen patients under evaluation for Cushing's syndrome (Cushing's disease, n = 12; ectopic ACTH syndrome, n = 2; glucocorticoid resistance, n = 1; hormonally inactive adenoma, n = 1) were catheterized. Two of the patients with Cushing's disease received 4.0 mg naloxone iv 15 min before stimulation with CRH. Patients with Cushing's disease demonstrated a central/peripheral gradient and an intersinus gradient not only for ACTH, but also for PRL, alpha-subunit, GH, and TSH, provided that the latter two hormones were not completely suppressed by the glucocorticoid excess. Moreover, all hormones increased in response to CRH on the side with the highest ACTH concentration; PRL rose from 31.2 +/- 6.4 to 61.6 +/- 12.4 micrograms/L (P less than 0.01), and alpha-subunit from 2.6 +/- 0.6 to 6.4 +/- 1.7 micrograms/L, (P less than 0.01). Naloxone was unable to abolish the PRL or alpha-subunit increase in response to CRH. A multihormonal response to CRH in inferior petrosal sinus blood was also observed in the patient with glucocorticoid resistance and in the patient with the hormonally inactive tumor, but not in the patients with ectopic ACTH secretion. The multihormonal response to CRH could be explained by cosecretion of other hormones together with ACTH from corticotroph adenoma, by an effect of CRH on pituitary blood flow, or by a paracrine action of pituitary corticotrophs on adjacent normal pituitary cells. Our results do not support the concept that such a paracrine action is mediated by beta-endorphin. However, a higher dose of naloxone may be required to antagonize the action of pituitary beta-endorphin.
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PMID:A multihormonal response to corticotropin-releasing hormone in inferior petrosal sinus blood of patients with Cushing's disease. 169 62

Hormones of the hypothalamo-pituitary-adrenocortical (HPA-) axis are considered to be of physiological and clinical relevance in regulating spontaneous growth hormone (GH) secretion. To further investigate interdependencies between both systems, we studied the effects of adrenocorticotropin [ACTH(1-24)] and human corticotropin-releasing hormone (h-CRH) upon spontaneous GH secretion in 10 male volunteers. Administration of 1 microgram ACTH (1-24), 10 micrograms h-CRH or saline (control: CTL) every hour from 9.00 to 6.00 p.m. resulted in significant differences of cortisol secretion during the entire observation period (8.00 a.m.-3.00 a.m.) between the three groups (p less than 0.001, Friedman two-way ANOVA). Mean area under the time course curve (AUC) values (+/- SEM) for cortisol expressed as ng x 1,000 x min/ml showed also significant differences between the three treatments from 8.00 a.m. to 3.00 a.m.: CTL 64.0 +/- 6.4, ACTH(1-24) 178.5 +/- 9.4 (p less than 0.01, Wilcoxon test), h-CRH 88.5 +/- 5.6 (p less than 0.01). The main portion of cortisol was released during daytime from 8.00 a.m. to 11.00 p.m., where the most significant differences in the AUC values emerged: CTL 59.6 +/- 5.8, ACTH(1-24) 171.5 +/- 8.8 (p less than 0.01, Wilcoxon test), h-CRH 80.2 +/- 5.1 (p less than 0.01). With regard to GH secretion, significant differences became obvious between the three treatments during daytime from 8.00 a.m. to 11.00 p.m. and the sleep-related period from 11.00 p.m. to 3.00 a.m. (p less than 0.01 and p less than 0.02, Friedman two-way ANOVA).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of human corticotropin-releasing hormone and adrenocorticotropin upon spontaneous growth hormone secretion. 174 61

Increased knowledge on the mechanisms whereby corticotropin releasing hormone (CRH) and opioid peptides mediate the effects of stress has helped us to understand the relationship between stress and disturbed reproductive function. Increases of CRH and beta-endorphin in the hypothalamus in stressful situations inhibits the secretion of gonadotropins, oxytocin and vasopressin. This may lead to amenorrhea, which often is a consequence of intensive training or psychological stress, or it may disrupt parturition and lactation. There is a relationship between ovarian function and opioid peptides in the hypothalamus. Opioid peptides increase during puberty and fall at the menopause. Oestradiol and progesterone increase beta-endorphin concentrations in the luteal phase of the menstrual cycle, and this is followed by a rapid fall at menstruation. These changes may mediate symptoms typical of the premenstrual syndrome. Rather intensive exercise is required to increase plasma concentrations of beta-endorphin and corticotropin. During labour the amounts of beta-endorphin and corticotropin reach the values found in athletes during maximal exercise. The placenta produces increasing amounts of CRH towards the end of pregnancy which may help the mother and fetus to withstand the increased demands of labour. The placenta may thus be involved in the adaptation of the stress mechanism during pregnancy. CRH has also a paracrine function in different biological processes of the placenta and fetal membranes. It is possible to counteract the deleterious effects of stress on reproductive function by the administration of opiate antagonists. Induction of ovulation with naltrexone has been shown in patients with hypothalamic amenorrhea but the effect on fertility is not known.
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PMID:Corticotropin-releasing hormone and opioid peptides in reproduction and stress. 175 18

The opioid peptide, beta-endorphin, originates from proopiomelanocortin (POMC) under the influence of corticotropin releasing hormone (CHR). It increases the threshold of pain and has a certain influence on the formation of hypophyseal hormones, especially in stress. It is found that beta-endorphin stimulates the secretion of prolactin, a growth hormone, and vasopressin; it inhibates formation of follicle-stimulating and luteinizating hormones, oxytocin and dopamine, and gonadotropin, a releasing hormone. The process of acetylization decreases its activity. The results of experimental trials revealed that acetylisation in the foetal period was absent. The aim of the study was to define beta-endorphin concentration during normal vaginal labor and Cesarean section. Samples of peripheral blood of patients with spontaneous vaginal labor (n = 15) and of those in whom labor was operatively terminated (Cesarean section) (n = 10), were analysed. Values of this opiate were determined in the umbilical cord of newborn infants, in the amniotic fluid and placental compartment. The obtained results were statistically analysed. In intrapartum beta-endorphins were significantly increased reaching the highest level during expulsion (326 pg/ml); in the placental compartment these values were higher (in retroplacental blood 514 pg/ml) reaching the highest value of 917 pg/ml, p less than 0.01 in the placenta. In Cesarean section beta-endorphin values in the peripheral blood showed no significant differences during spontaneous vaginal labor. However, increased values of this natural opiate were observed six hours after surgery. Beta-endorphin concentrations in the placental compartment and the placenta during normal vaginal labor were significantly higher in comparison with labor by Cesarean section (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The opioid peptide, beta-endorphin, in spontaneous vaginal delivery and cesarean section]. 180 97

1. The possible correlation between secretions of adrenocorticotropic hormone (ACTH) and of beta-lipotropin (beta-LPH), two pro-opiomelanocortin (POMC)-derived peptides, was investigated in 27 normal subjects under basal conditions (circadian rhythm), after the administration of 1 mg dexamethasone and in tests involving acute (human corticotropin releasing hormone, hCRH, and insulin tolerance test, ITT) and chronic (metyrapone) stimulation. 2. All subjects presented circadian rhythm and an operating negative feedback mechanism. Plasma ACTH and beta-LPH concentrations were correlated in all tests. The increase in ACTH and beta-LPH levels after hCRH was lower than that detected after ITT, though both increases were more discrete than those detected after stimulation with metyrapone. 3. The data suggest that, under hypoglycemic conditions, ACTH and beta-LPH secretion involves other POMC secretagogues in addition to endogenous CRH. The nature of these factors remains undefined. The greater efficacy of metyrapone treatment in elevating ACTH and beta-LPH levels is most likely mediated by sustained reduction in cortisol production and interruption of the rapid steroid feedback on the pituitary. 4. The molar peak ratios of the acute tests, which were similar to one another, differed from the peak ratio obtained during the metyrapone test, suggesting that corticotrophs may present pools with differentiated ACTH and beta-LPH content and release according to the type and/or duration of the stimulus.
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PMID:Beta-lipotropin/adrenocorticotropic hormone responses to corticotropin releasing hormone, hypoglycemia, metyrapone and dexamethasone in normal human subjects. 196 79

Although somatostatin inhibits a variety of pituitary and non-pituitary hormones, not univocal data on its effects on ACTH release have been reported so far. In this study we investigated the effects of somatostatin or octreotide on ACTH levels of patients with corticotropin hypersecretion: 7 patients with Addison's disease, 2 patients previously adrenalectomized for Cushing's disease, 4 patients with Cushing's disease and 3 patients with ectopic ACTH syndrome. Plasma ACTH and cortisol levels were determined after somatostatin (500 micrograms over 60 min) infusion or octreotide (100 micrograms sc) injection. In 5 other patients with Cushing's disease ACTH and cortisol responses to CRH (1 microgram/kg iv) were evaluated in basal conditions and after octreotide acute administration. In no patients with Addison's disease any inhibitory influence of somatostatin (delta % = -21, -25) or octreotide (delta % = -38 +/- 12 vs -39 +/- 12 after saline) on plasma ACTH was found. Somatostatin did not significantly inhibit plasma ACTH in the two patients previously adrenalectomized for Cushing's disease and in 3 patients with Cushing's syndrome; in other 4 patients with Cushing's syndrome octreotide did not affect plasma ACTH levels. In 5 patients with Cushing's disease the plasma ACTH and cortisol responses to CRH were similar both before (ACTH from 9.9 +/- 1.7 pmol/L to 19.4 +/- 6.1 pmol/L; cortisol from 496 +/- 43.9 nmol/L to 923 +/- 355 nmol/L) and after octreotide injection (ACTH from 8.8 +/- 2.4 pmol/L to 19.1 +/- 8.2 pmol/L; cortisol from 510 +/- 54.6 nmol/L to 735 +/- 220 nmol/L). In conclusion, the acute administration of somatostatin or octreotide is not able to modify ACTH levels in patients with corticotropin hypersecretion either due to hypocortisolemic state or consequent to ACTH-secreting pituitary or ectopic tumors; moreover, octreotide does not affect the pituitary-adrenal responsiveness to CRH in patients with Cushing's disease.
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PMID:Failure of somatostatin and octreotide to acutely affect the hypothalamic-pituitary-adrenal function in patients with corticotropin hypersecretion. 197 78


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