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)

Three trials were conducted to investigate plasma corticosterone (B) levels in Large White turkey hens in response to adrenocorticotropic hormone (ACTH) injections at different ages, doses, and routes of administration. In Trial 1, hens were subjected to one of the following treatments at 10, 15, and 20 wk of age: cold water immersion (5 C for 1 min), ACTH injection (10 IU/kg), or saline injection. The plasma B responses to ACTH and cold water immersion followed the same general pattern in all three age groups. Plasma B levels of hens in the ACTH treatment were depressed below control B levels until 6 h postinjection, when they became elevated. Plasma B levels of hens in the cold water treatment were either similar to or increased above those of controls by 2 h posttreatment and were depressed below control levels at .5 h posttreatment at 10 and 15 wk of age. In Trial 2, three dose levels of ACTH (1, 5, and 10 IU/kg) were injected either intramuscularly (IM) or intravenously (IV) in 10-wk-old hens. There was both a dose and route of administration effect. Of the IM-injected hens, only those in the 1-IU ACTH treatment group had significantly (P less than .05) increased plasma B levels and this occurred 4 h postinjection. However, plasma B levels of the 1 and 5-IU IV-ACTH treatment hens were significantly (P less than .05) elevated at .5 h postinjection. Plasma B of the 10-IU IM and IV-ACTH treatments were consistently, but not significantly, lower than controls through 4 h postinjection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma corticosterone response of turkeys to adrenocorticotropic hormone: age, dose, and route of administration effects. 282 52

Normal human pituitaries were extracted in boiling water and acetic acid, and the alpha-amidated peptide products of pro-opiomelanocortin (POMC), alpha-melanocyte-stimulating hormone (alpha MSH), gamma-melanocyte-stimulating hormone (gamma 1MSH), and amidated hinge peptide (HP-N), as well as their glycine-extended precursors, were characterized by sequence-specific radioimmunoassays, gel-chromatography, h.p.l.c. and amino acid sequencing. alpha MSH and gamma 1MSH constituted 0.27-1.32% and 0.10-5.10%, respectively, of the POMC-derived products [calculated as the sum of adrenocorticotropic hormone (ACTH)-(1-39), ACTH-(1-14) and alpha MSH immunoreactivity]. alpha MSH and ACTH-(1-14) were only present in non- or mono-acetylated forms. Only large forms of gamma 1MSH and gamma 2MSH were present in partly glycosylated states. The hinge peptides were amidated to an extent two to three orders of magnitude greater than alpha MSH and gamma 1MSH. Most (99%) of the HP-N was of low molecular mass and consisted mainly of HP-N-30. The remaining part was high-molecular-mass HP-N, probably HP-N-108, although the presence of HP-N-44 could not be completely excluded. These results show that all the possible amidated POMC-related peptides are present in normal human pituitary. It also shows that cleavage in vivo at all dibasic amino acids but one, takes place at the N-terminal POMC region; the exception is at the POMC-(49-50) N-terminal of the gamma MSH sequence. The pattern of peptides produced suggests that the generation of amidated peptides is mainly regulated at the endopeptidase level.
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PMID:Alpha-amidated peptides derived from pro-opiomelanocortin in normal human pituitary. 283 46

A toxicology study was performed in mice given a superpotent alpha melanocyte stimulating hormone (MSH) analog. This 13 amino acid derivative, [Nle4, D-Phe7]alpha-MSH or NDP-MSH, is a melanotropin which is very slowly biodegraded in vivo and is active at 1/1,000 the concentration of natural alpha-MSH. Mice were administered up to 2 mg/kg of the analog daily and weekly over 4 or 12 weeks by both topical application (in 90% DMSO) or by IP injections (in physiologic saline). At the end of this period, no toxic effects were observed in various organs, on hematologic indices, or on weight gain. A slight increase in triglyceride and platelet levels were noted in mice given the analog weekly for 12 weeks. There was no evidence of an effect on behavior nor ACTH-like endocrine actions such as elevated serum cortisol levels. Transdermal drug delivery studies performed in vitro showed reproducible diffusion of the NDP-MSH analog through full-thickness mouse skin. Approximately 0.002% to 0.05% of a 10(-4) M preparation was transdermally delivered using a DMSO/water solution or a PEG/alcohol cream base, respectively. This superpotent analog is now entering a Phase I clinical trial with possible therapeutic applications for the treatment of hypomelanotic disorders such as vitiligo and for pharmacologic tanning without the need for sunlight exposure.
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PMID:Toxicologic studies of a superpotent alpha-melanotropin, [Nle4, D-Phe7]alpha-MSH. 285 52

Endocrine and thermoregulatory responses were studied in male rats exposed to heat (32.5 +/- 0.1 degrees C) from acclimation temperatures of either 24.5 +/- 0.1 degrees C or 29.2 +/- 0.1 degrees C. After 1 hr in the heat, evaporative water loss and tail skin temperature changes in the 24.5 degrees C acclimated rats were greater than in the 29.2 degrees C acclimated rats; both groups displayed similar changes in metabolic rate and rectal temperature. At the respective acclimation temperatures, 29.2 degrees C rats displayed lowered plasma thyroid hormones, elevated beta-endorphin-like immunoreactivity (beta-END-LI) in the plasma, neurointermediate and anterior lobes of the pituitary gland, and no change in plasma corticosterone levels compared to 24.5 degrees C rats. After exposure to 32.5 degrees C for 1 hr, both groups of rats maintained similar plasma corticosterone levels; however, only the 24.5 degrees C group increased plasma thyroxine and beta-END-LI. These data suggest that beta-endorphin may be involved in body temperature regulation during acclimation to elevated environmental temperatures.
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PMID:The effects of acclimation temperature on pituitary and plasma beta-endorphin in rats at 32.5 degrees C. 286 99

The levels of dynorphin, alpha-neoendorphin and beta-endorphin immunoreactivity (ir-DYN, ir-alpha-NEO, ir-beta-E) were measured in the brain, pituitary and gut of rats subjected to a variety of manipulations. Water deprivation caused an increase in the ir-DYN and ir-alpha-NEO content in the hypothalamus and a decrease in the neurointermediate (NI) lobe of the pituitary. The ir-beta-E level decreased in the hypothalamus and anterior lobe of the pituitary, while it increased in the NI-pituitary. Food deprivation, as well as chronic fenfluramine (10-20 mg/kg) treatment increased, while acute muscimol (0.5 micrograms/10 microliter) treatment decreased the ir-beta-E, but not ir-DYN or ir-alpha-NEO content in the hypothalamus. The anterior pituitary content of ir-beta-E was increased after food deprivation and decreased after chronic fenfluramine treatment. However, the ir-DYN and ir-alpha-NEO contents in the duodenum were markedly increased after food deprivation, while chronic fenfluramine treatment led to a dramatic decrease in the ir-DYN content. These results suggest that the levels of opioid peptides in the brain, pituitary and gut may be differentially and independently affected by alteration of the ingestive behavior.
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PMID:Brain and peripheral opioid peptides after changes in ingestive behavior. 286 26

These experiments were designed to identify brain sites at which opioids might act to influence ingestive behavior and to determine which opioid receptor types are involved. After food deprivation, rats were given microinjections of naloxone into several brain regions and food intake was measured. Injections into or near the paraventricular (PVN) or ventromedial (VMH) hypothalamic nuclei or the globus pallidus (GP) reduced food intake; injections into the striatum or lateral hypothalamus (LH) were ineffective. A second study examined the ingestive effects of roughly equimolar doses (1.43-1.75 nmol) of dynorphin A (DYN), beta-endorphin (beta-END), and D-Ala2,D-Leu5-enkephalin (DADLE) when injected into 4 different brain regions. Only DYN significantly increased food intake, and this effect was seen only with injections into the PVN and VMH. Beta-END stimulated water intake when injected into the PVN, VMH and GP but not the LH. Further studies indicated that with PVN injections, DYN was effective at a dose as low as 0.47 nmol, and that a higher dose of DADLE (4.39 nmol) did stimulate food intake. These studies support an important role for dynorphin and the kappa opioid receptor in the regulation of feeding and suggest that the opioid regulation of food and water intake can be differentiated both by sites of action and by effective agonists.
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PMID:Opioid-induced feeding: localization of sensitive brain sites. 287 Jul 73

The neuroanatomical distribution of dynorphin B-like immunoreactivity (DYN-B) was studied in the adult male and female albino rat. The distribution of DYN B in colchicine- and noncolchicine-treated animals was also compared to that of another opioid peptide derived from the prodynorphin precursor dynorphin A (1-8) (DYN 1-8), and an opioid peptide derived from the proenkephalin precursor met-enkephalin-arg-gly-leu (MERGL). DYN B cell bodies were present in nonpyramidal cells of neo- and allocortices, medium-sized cells of the caudate-putamen, nucleus accumbens, lateral part of the central nucleus of the amygdala, bed nucleus of the stria terminalis, preoptic area, and in sectors of nearly every hypothalamic nucleus and area, medial pretectal area, and nucleus of the optic tract, periaqueductal gray, raphe nuclei, cuneiform nucleus, sagulum, retrorubral nucleus, peripeduncular nucleus, lateral terminal nucleus, pedunculopontine nucleus, mesencephalic trigeminal nucleus, parabigeminal nucleus, dorsal nucleus of the lateral lemniscus, lateral superior olivary nucleus, superior paraolivary nucleus, medial superior olivary nucleus, ventral nucleus of the trapezoid body, lateral dorsal tegmental nucleus, accessory trigeminal nucleus, solitary nucleus, nucleus ambiguus, paratrigeminal nucleus, area postrema, lateral reticular nucleus, and ventrolateral region of the reticular formation. Fiber systems are present that conform to many of the known output systems of these nuclei, including major descending pathways (e.g., striatonigral, striatopallidal, reticulospinal, hypothalamospinal pathways), short projection systems (e.g., mossy fibers in hippocampus, hypothalamo-hypophyseal pathways), and local circuit pathways (e.g., in cortex, hypothalamus). The distribution of MERGL was, with a few notable exceptions, in the same nuclei as DYN B. From these neuroanatomical data, it appears that the dynorphin and enkephalin peptides are strategically located in brain regions that regulate extrapyramidal motor function, cardiovascular and water balance systems, eating, sensory processing, and pain perception.
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PMID:Distribution of dynorphin and enkephalin peptides in the rat brain. 287 59

Bilateral, radiofrequency lesions of the mediobasal arcuate hypothalamus (MBH) strongly depleted levels of immunoreactive (ir)-beta-endorphin (beta-EP) in the hypothalamus and other brain tissues: these changes reflect destruction of those beta-EP-containing perikarya which are located in the MBH. No change in plasma ir-beta-EP was seen. The ir-dynorphin (DYN) content of the hypothalamus was also depressed while that of ir-Met-enkephalin was unaffected. The fall in hypothalamic ir-beta-EP was correlated with the fall in that of ir-DYN. Lesioned rats displayed only a minor, transient reduction in rate of weight gain between days 3 and 9 postsurgery: this disappeared thereafter. Further, the lesion did not affect the pattern of weight loss and regain associated with 24 h food and water deprivation. Indeed, the total 24 h (daily) food intake (FI) and water intake (WI) of lesioned rats did not differ from that of sham animals while deprivation-induced hyperphagia and hyperdipsia was not attenuated by the lesions. Moreover, the ability of naltrexone to decrease FI and WI (during both dark and light phases of the daily cycle) was not altered by the lesions. These observations indicate that central beta-EP may not be essential for the maintenance of a normal 24 h FI and WI and that opioid antagonists do not act upon the MBH or upon central beta-EP neurones in their suppression of FI and WI. Further, they suggest that central beta-EP may not fulfil an essential role in the control of body weight in the rat. Lesioned rats did, however, reveal a shift in the diurnal rhythmicity of FI and WI reflected in a reduction in the dark:light ratios of these. An alteration in the diurnal rhythmicity of sleeping and core temperature, but not locomotor activity, was also seen. The shifts in hypothalamic ir-beta-EP and ir-DYN (but no other tissue levels of any peptide) were correlated with the magnitude of the shifts in diurnal rhythmicity of ingestive behaviour. Moreover, lesions caudal to the MBH (not affecting hypothalamic ir-beta-EP or ir-DYN) or dexamethasone treatment (which affects pituitary pools of ir-beta-EP and ir-DYN) did not modify these rhythms. Thus, in these respects, the effects are 'particular' to MBH lesions modifying hypothalamic ir-beta-EP and ir-DYN. The data suggest that the MBH may play a role in the modulation of the diurnal scheduling of ingestive behaviour in the rat.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The role of the mediobasal arcuate hypothalamus in relation to opioid systems in the control of ingestive behaviour in the rat. 287 65

The brain acetone powders of the sea snakes Hydrophis cyanocinctus and Lapemis hardwickii were extracted with a mixture of acetone:water:hydrochloric acid (40:21:1 by volume) and the extracts were then added to a copious volume of acetone, in accordance with the method of C. H. Li (1952, J. Amer. Chem. Soc., 74, 2134) for preparing adrenocorticotropin and beta-endorphin from mammalian pituitaries. The resultant precipitate, designated acid acetone powder, possessed adrenocorticotropic activity as evidenced in its ability to stimulate corticosterone production in isolated rat adrenal decapsular cells and lipolysis in isolated hamster adipocytes, and in its cross-reactivity in an ACTH radioimmunoassay. The presence of opioid molecules was indicated by activity in opiate radioreceptor assay using either 3H-D-Ala2-D-Leu5 enkephalin or [3H]naloxone as ligand and rat brain membranes. The brain acetone powders possessed neither "lactogenic" nor "somatogenic" activity as evidenced by their inability to displace the primary ligand in the rat hepatic prolactin receptor- and growth hormone receptor-binding assays, respectively.
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PMID:Evidence for the presence of adrenocorticotropic and opiate-like hormones in the brains of two sea snakes, Hydrophis cyanocinctus and Lapemis hardwickii. 287 27

Male rats were injected s.c. once daily during the first week of life with beta-endorphin (BE), morphiceptin, the antiopiate Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH2), or one of the two opiate peptides in combination Tyr-MIF-1. Pups treated with neonatal BE removed their tails from a series of increasingly hot water baths significantly faster than controls on day 9, confirming our earlier studies. In addition, we found that Tyr-MIF-1 blocked this effect of BE. At 4.5 months, latency to lick a hindpaw in the hot-plate test was significantly faster in groups given BE alone, morphiceptin alone, or the control vehicle than in any of the 3 groups given Tyr-MIF-1. At 6 months the two groups given opiate peptides alone showed faster tail-flick latencies than the controls and the groups given Tyr-MIF-1. These results indicated that the long-term nociceptive changes induced by the opiate peptides were opposite to those induced by Tyr-MIF-1. Mean tail-flick latencies of the groups on day 9 correlated well with hot-plate and tail-flick scores in adulthood, indicating that the effects of the peptides were persistent. The neonatal peptide treatments did not differentially affect the analgesia induced by the stress of footshock or warm-water swim. Rats given either of the opiate peptides alone tended to fall off a rotorod faster than those in the other groups. These results support the role of Tyr-MIF-1 as an antiopiate and further illustrate the long-term effects of neonatally administered peptides.
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PMID:Long-term hyperalgesia induced by neonatal beta-endorphin and morphiceptin is blocked by neonatal Tyr-MIF-1. 288 15


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