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)

mRNA that encodes the common peptide precursor for the hormones corticotropin and beta-lipotropin was purified from the neurointermediate lobe of bovine pituitaries, and double-stranded cDNA species synthesized from this template were cloned in Escherichia coli X1776 by inserting them into the Pst I endonuclease cleavage site of the pBR322 plasmid using poly(dG)poly(dC) homopolymeric extensions. Certain of the cloned cDNA inserts contain nucleotides corresponding to the complete amino acid sequence of bovine corticotropin and a coding sequence that corresponds to at least the first portion of bovine beta-lipotropin. The nucleotide sequences coding for corticotropin and beta-lipotropin are separated on the cDNA by a 6-base-pair sequence encoding lysine and arginine, indicating that the carboxyl terminus of corticotropin is connected on the precursor peptide with the amino terminus of beta-lipotropin by these two amino acids. In addition, the cloned cDNA insert is characterized by an unusually high C+G nucleotide base content as well as by a number of DNA sequence duplications.
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PMID:Construction of bacterial plasmids that contain the nucleotide sequence for bovine corticotropin-beta-lipotropin precursor. 21 7

Using a specific radioimmunoassay the concentrations of beta-endorphin, beta-lipotropin and corticotropin in maternal plasma were studied during pregnancy and in the early puerperium. Compared with the values in nonpregnant women, levels of beta-endorphin and beta-lipotropin were slightly lower in the first and second trimesters; corticotropin showed no difference in the first trimester. The concentrations of all these peptides increased towards term, most markedly in the case of corticotropin. The diurnal variation was studied near term and again in the early puerperium. beta-Endorphin and corticotropin showed a parallel diurnal variation. The values in the morning and during the day were slightly higher during pregnancy than in the puerperium, whereas the values at midnight were similar. After vaginal delivery, a rapid and parallel decrease in the plasma levels of beta-endorphin, beta-lipotropin and corticotropin was found. In elective cesarean section, the values were highest 30 min after delivery, reflecting surgical stress, and then the decrease was similar to that after vaginal delivery. Thus parallel changes in the plasma levels of beta-endorphin, beta-lipotropin and corticotropin during pregnancy and in the early puerperium were found, which can be explained by their origin from a common precursor peptide, pro-opiomelanocortin. The rise in the plasma levels of corticotropin and endorphins near term and the exaggerated diurnal variation is probably a reflection of a maternal adaptation to stress.
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PMID:Plasma levels and diurnal variation of beta-endorphin, beta-lipotropin and corticotropin during pregnancy and early puerperium. 282 31

The biosynthesis of human corticotropin (ACTH) was studied in organ culture of pituitary adenomas and by translating mRNA from an ectopic ACTH-producing tumor in a cell-free system. Peptides similar to human ACTH, beta-lipotropin, and the amino-terminal glycopeptide are cleaved from a common precursor with an apparent molecular weight of 35,000 on sodium dodecyl sulfate/polyacrylamide gels. The precursors synthesized in pituitary and ectopic ACTH-producing tissues are indistinguishable. The cleavage sites of the peptide chain appear to be similar to those previously deduced for murine and bovine ACTH. Immunoprecipitation studies suggest that the primary structure of the precursor peptide is similar in all three species. However, glycosylation is different in the human and murine precursors: the precursor to human ACTH appears to be glycosylated only in the amino-terminal fragment, not in the ACTH or beta-lipotropin sequences. Studies with an autopsied normal human pituitary suggest that neither normal nor adenomatous pituitary tissue glycosylates the ACTH sequence.
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PMID:Processing of the precursor to corticotropin and beta-lipotropin in humans. 625 67

The association of acanthosis nigricans with pituitary tumors and insulin-resistant diabetes suggests that a pituitary peptide may promote papillomatosis and acanthosis characteristic of acanthosis nigricans. Although such a peptide has not been isolated, it may derive by sequential cleavage from the 31,000-dalton precursor peptide to ACTH and beta-lipotropin (beta-LPH). In order to evaluate the role of pituitary peptides in the pathogenesis of acanthosis nigricans, we compared plasma levels of beta-endorphin (beta-EP) and ACTH in plasma of 8 fasting patients with obesity-associated benign acanthosis nigricans and 7 fasting normal controls utilizing sensitive radioimmunoassay procedures. Mean plasma beta-EP levels for the acanthosis nigricans and control subjects were not significantly different (90 pg/ml vs. 140 pg/ml), nor was any significant difference observed between plasma ACTH levels of the 2 groups (42.3 and 31.2 pg/ml, respectively.) Our data indicate that plasma levels of the pituitary-derived peptides ACTH and beta-EP are not increased in obesity-associated benign acanthosis nigricans, and suggest that its proposed hormonal mediator might originate independently from the large peptide precursor of ACTH, beta-LPH and their fragments.
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PMID:Neuropeptides in the pathogenesis of obesity-associated benign acanthosis nigricans. 629 89

[he concentrations of immunoreactive (ir-) peptides derived from the opioid peptide precursors proenkephalin A (Met-enkephalin), proenkephalin B [dynorphin (DYN)-(1-17), dynorphin-(1-8), dynorphin B, alpha-neoendorphin (alpha-NEO-E), beta-NEO-E] and proopiomelanocortin [beta-endorphin (beta-END)], and of the neurosecretory hormones vasopressin and oxytocin increased between approximately 10-fold and 50-fold from birth to adulthood in the rate hypothalamus. Gel filtration and HPLC analysis of proenkephalin B-derived opioid peptides revealed that in 3-day-old rats the predominant portion of ir-dynorphin-(1-17) and a substantial part of ir-dynorphin B consisted of a high (6000) mol wt species, a common precursor peptide for DYN-(1-17) and DYN B. In adults rats, however, authentic DYN-(1-17) and DYN B were found to be the major ir-forms. The mol wt patterns of ir-DYN-(1-8), ir-alpha-NEO-E and ir-beta-NEO-E did not differ between 3-day-old and adult rats and reflected predominantly the respective authentic opioid peptides. Taking into consideration the developmental changes in the mol wt pattern of ir-DYN-(1-17), authentic DYN-(1-17) was 5 times lower in concentration than DYN-(1-8) in 3-day-old rats, whereas in adults these opioid peptides occurred in equimolar concentrations. These findings suggest that the posttranslational processing of the precursor proenkephalin B changes in the course of postnatal development. Ir-beta-END in the hypothalamus of newborn and adult rats consisted exclusively of beta-END-sized peptides which were not (unlike those in the intermediate pituitary lobe) alpha-N-acetylated. Thus, in the hypothalamus, the enzymatic processing of the opioid peptide precursor proopiomelanocortin to beta-END seems to be fully active at birth, in contrast to that of proenkephalin B.
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PMID:Evidence for a differential postnatal development of proenkephalin B (= prodynorphin)-derived opioid peptides in the rat hypothalamus. 654 67

In conscious and urethane-anesthetized rats intravenously (i.v.) administered gamma 2-melanocyte-stimulating hormone (gamma 2-MSH), a melanotropin derived from the precursor peptide pro-opiomelanocortin (POMC), has been shown to induce a pressor response combined with a tachycardia. A site of action within the hindbrain, e.g. the nucleus tractus solitarii (NTS) or the area postrema (AP), has been suggested. In order to test the postulate that gamma 2-MSH acts within these hindbrain regions, the peptide was microinjected into various parts of the NTS and into the AP of urethane-anesthetized rats and blood pressure (BP) and heart rate (HR) were measured. Injection of gamma 2-MSH (100-500 pmol) into the NTS resulted in a dose-dependent decrease in BP and HR rather than in the expected pressor and tachycardiac response which is generally found in conscious and urethane-anesthetized rats following i.v. administration of the peptide. With respect to the depressor and bradycardiac effect the melanotropin was far more potent when injected into the pars commissuralis than into the medial part of the NTS. The responses were maximal after 3-4 min and lasted for about 15 min. gamma 2-MSH had no effect when injected into the AP. It is noteworthy that also a hypotensive and bradycardic effect for gamma 2-MSH is found in pentobarbital-anesthetized rats following i.v. administration. Therefore, we conclude that in addition to a pressor and tachycardic response gamma 2-MSH can elicit an opposite effect by interaction with structures within a discrete region in the NTS, the pars commissuralis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A hypotensive and bradycardic action of gamma 2-melanocyte-stimulating hormone (gamma 2-MSH) microinjected into the nucleus tractus solitarii of the rat. 813

Chronic food restriction decreases secretion of LH as a result of inhibitory influences on secretion of LHRH. We have previously reported that neuropeptide-Y (NPY) may directly or indirectly mediate this inhibitory effect on LHRH secretion. In the study reported here, we tested the hypothesis that long-term food restriction suppresses tonic release of LH as a result of 1) an increase in biosynthetic activity of NPY neurons in the arcuate nucleus of the hypothalamus, 2) an increase in activity of neurons that secrete beta-endorphin, and 3) a decrease in biosynthesis of LHRH. To test predictions of the hypothesis, we compared levels of mRNA encoding NPY, proopiomelanocortin (POMC; the precursor peptide of beta-endorphin), and LHRH, as well as tonic secretion of LH in food-restricted and well-nourished ewe lambs. Ten ewe lambs were ovariectomized at 18 wk of age and randomly assigned to receive either 100% nutritional requirements (FED; n = 5), or 30% requirements (R; n = 5) between 18 and 25 wk of age. At 25 wk of age, blood samples were taken every 10 min for 6 h and assayed for LH. The tonic release of LH in R lambs was less than that of FED lambs. Hypothalami were collected 4 days after blood sampling and sectioned at 12 microns for use in in situ hybridization. Radiolabeled molecular probes specific for mRNAs encoding NPY, POMC, or LHRH were hybridized to hypothalamic tissue sections. Levels of NPY mRNA were 88% greater in R vs. FED lambs (p < 0.01), whereas levels of POMC mRNA were 52% lower in R vs. FED lambs (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of food restriction on neuropeptide-Y, proopiomelanocortin, and luteinizing hormone-releasing hormone gene expression in sheep hypothalami. 821 49

In elderly women with proximal femur fractures, plasma cortisol levels are still elevated 2 weeks after injury. We have now measured the concentrations of adrenocorticotrophin (ACTH) and its precursor peptides (pro-opiomelanocortin plus pro-ACTH) in blood samples obtained in the morning and afternoon from such patients and from old and young control subjects. In healthy subjects, aging had no effect on these variables. Compared with healthy elderly women, the injured women had elevated cortisol but not ACTH concentrations; at both times of day their precursor peptide concentration was increased but probably not enough to affect cortisol secretion substantially. There were no correlations between the concentrations of cortisol, ACTH, and precursor peptides. We have also studied adrenocortical sensitivity after giving dexamethasone overnight. The cortisol responses to graded doses of ACTH did not differ between injured and healthy elderly women, suggesting that their higher cortisol concentrations were the results of stimuli acting independently of ACTH.
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PMID:Factors influencing cortisol-adrenocorticotrophin relationships in elderly women with upper femur fractures. 838 90

Melanocortin-4 receptor (MC4-R) density is thought to be regulated by synaptic availability of endogenous agonist, alpha-melanocyte-stimulating hormone (alpha-MSH), and also by agouti-related protein (AGRP), which acts as a competitive antagonist. As hypothalamic MC4-R have been implicated in the regulation of energy balance, we examined concentrations of alpha-MSH and AGRP in hypothalami of dietary-obese and food-restricted rats. In dietary-obese rats, AGRP concentrations were significantly increased by 43% (p < 0.01) above lean controls, whereas a 91% (p < 0.01) reduction was observed in food-restricted rats. Surprisingly, hypothalamic concentrations of alpha-MSH and its precursor peptide, pro-opiomelanocortin (POMC), did not differ significantly from controls in either model. In conclusion, we suggest that MC4-R activity may not be regulated by changes in agonist (alpha-MSH) but by changes in the antagonist (AGRP) availability, which may modulate background activation of the receptor by tonic alpha-MSH release. AGRP may be an important modulator of feeding behaviour.
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PMID:Changes in hypothalamic agouti-related protein (AGRP), but not alpha-MSH or pro-opiomelanocortin concentrations in dietary-obese and food-restricted rats. 1032 27

The opioid peptide, Orphanin FQ/nociceptin (OFQ/N(1-17))(,) its active fragments, and a related precursor peptide each produce analgesia following microinjection into the amygdala of rats. OFQ/N(1-17)-induced analgesia elicited from the amygdala is blocked by amygdala pretreatment of either general, mu, kappa, or delta-opioid antagonists even though OFQ/N(1-17) binds poorly to these receptor subtypes, and the antagonists bind poorly to the ORL-1/KOR-3 receptor. Agonists at mu and kappa opioid receptors as well as beta-endorphin each produce analgesia elicited from the amygdala that is blocked by opioid antagonist pretreatment in the ventrolateral periaqueductal gray (vlPAG) of rats. The present study examined whether pretreatment of general and selective opioid antagonists in the vlPAG blocked OFQ/N(1-17)-induced analgesia on the tail-flick test elicited from the amygdala, and whether pretreatment of general and selective opioid antagonists in the amygdala blocked OFQ/N(1-17)-induced analgesia elicited from the vlPAG of rats. OFQ/N(1-17)-induced analgesia elicited from the amygdala was significantly and markedly reduced following vlPAG pretreatment with a dose range of either naltrexone, beta-funaltrexamine (beta-FNA, mu), nor-binaltorphamine (NBNI, kappa) or naltrindole (NTI, delta). In contrast, opioid antagonists administered into misplaced mesencephalic control placements ventral and lateral to the vlPAG actually enhanced OFQ/N(1-17)-induced analgesia elicited from the amygdala. OFQ/N(1-17)-induced analgesia elicited from the vlPAG was significantly and markedly reduced following amygdala pretreatment with naltrexone and NBNI, to a lesser degree by NTI, and was unaffected by beta-FNA. Yet, opioid antagonists administered into misplaced amygdala control placements were generally ineffective in altering OFQ/N(1-17)-induced analgesia elicited from the vlPAG. Latencies were transiently increased by general, but not selective opioid antagonist treatment alone in the amygdala, but not the vlPAG. These data indicate reciprocal and regional interactions between the amygdala and vlPAG in the mediation of OFQ/N(1-17) by classic opioid receptor subtype antagonists in rats.
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PMID:Reciprocal interactions between the amygdala and ventrolateral periaqueductal gray in mediating of Q/N(1-17)-induced analgesia in the rat. 1286 59


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