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)

The effect of synthetic MIF (H-Pro-Leu-Gly-NH2) on beta-MSH secretion was studied in five patients with Nelson's syndrome and in one patient with Addison's disease. Two milligrams of the tripetide were injected intravenously (1 mg in an acute injection, followed by a 30-minute-infusion of 1 mg in 20 ml of saline solution). No consistent effect could be observed during the 90-minute period after the beginning of the infusion. In the same patients, LVP stimulation and dexamethasone suppression tests brought about significant changes in the plasma beta-MSH and ACTH levels.
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PMID:Synthetic MIF has no effect on beta-MSH and ACTH hypersecretion in Nelson's syndrome. 0 86

Intrajugular administration of LHRH (0-6 and 1-2 mug) in hypophysectomized rats which received renal grafts of anterior pituitary induced a small but significant rise in plasma GH 5 and 10 min post-treatment. LHRH, at the same dose levels, was ineffective in weight-matched intact controls. MIF, at the dose of 1-2 mug, induced a slight GH rise 5 min after treatment in hypophysectomized trasnplanted rats, while it was ineffective in intact controls. Unlike the two hypothalamic peptides, alpha-MSH (0-6 and 1-2 mug) was ineffective as a GH-releaser in both transplanted and intact rats.
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PMID:Stimulation of growth hormone release by luteinizing hormone-releasing hormone and melanocyte-stimulating hormone-release inhibiting hormone in the hypophysectomized rat bearing an ectopic pituitary. 1 96

Previous reports have indicated that alpha-MSH release inhibiting hormone (MIF-1) increased the behavior occurring as a result of the dihydroxyphenylalanine (DOPA) potentiation test [3,7]. This study was undertaken to see whether dopamine (DA) or norepinephrine (NE) levels likewise increased in the test animals. The DOPA potentiation test was performed as follows: 2-4 hr before behavior measurement, 40 mg/kg of the monoamine oxidase inhibitor pargyline HCl was given orally. Two hr later this was followed by the intraperitoneal (IP) injection of MIF-1 at doses of 0.1, 0.3 or 1.0 mg/kg. Behavioral measurement was begun after the IP injection of 200 mg/kg of dl-DOPA 1-2 hr after the MIF-1. The parameters included social interaction, aggressiveness, fighting, ataxia, jumping, defecation, urination and salivation. The animals were beheaded while the behavior was still increased and the striatal area removed, placed in aluminum foil, and kept at -50 degrees C until assayed. In general, especially among the younger animals, a significant correlation (p=0.05 to p=0.01) was found between the increased behavioral responses to MIF-I and the rise in DA. Because of a few exceptions to this correlation the possibility is suggested that MIF-I might also affect behavior by acting directly on the postsynaptic membrane thus bypassing any change in NE or DA which is known to increase cycli AMP in the striatum.
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PMID:Possible association of increased rat behavioral effects and increased striatal dopamine and norepinephrine levels during the DOPA-potentiation test. 1 11

The intracarotid artery quick injection technique of Oldendorf was utilized to determine the Brain Uptake Index (BUI) of radio-labeled peptides in comparison with 3H2O or 14C-antipyrine as counterlabels. The normalized BUI values for 3H-MIF-I, 3H-alpha-MSH and 14C-AVP were 13.7, 9.6 and 13.0 respectively at 15 sec after injection consistent with their having readily penetrated the blood-brain barrier. The BUI values were similar, though somewhat increased, at 10 min postinjection consistent with their ready exit across the blood-brain barrier. At 15 sec after injection 0.5+/-0.1%/g brain of the originally injected peptide label was recovered; and 0.1+/-0.2%/g brain was recovered after 10 min. The label was distributed uniformly in the major brain regions at both times. However, the percentage of the originally injected label/g of pineal and pituitary gland tissue was 10-20 X increased as compared with the major brain regions as would be expected by their location outside the blood-brain barrier. The in vitro uptake of the radio-labeled peptides by synaptosomes prepared from the whole brain and the major brain regions was passive; it was not temperature dependent, nor was it Na+ dependent. However, the binding of the three peptides by the synaptosomes varied considerably: AVP greater than MSH greater MIF: 50 greater than 5 greater 1. The penetratin of the blood-brain barrier by the three peptides is consistent with their having CNS effects.
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PMID:Peptides readily penetrate the blood-brain barrier: uptake of peptides by synaptosomes is passive. 1 14

In 15 patients with congenital adrenal hyperplasia, the corticotrophic and melanotrophic functions were evaluated by plasma ACTH and beta-MSH radioimmunoassay. Evaluation of the corticotrophic and melanotrophic functions was also performed in 3 subjects after provocative tests (insulin-induced hypoglycaemia, metyrapone) and in 5 subjects after infusion of synthetic MIF (MSH-release inhibiting factor). The results indicate a significant increase in plasma ACTH and beta-MSH in CAH. In addition, we found that although in most cases there was a significant positive correlation between the plasma ACTH and beta-MSH levels, in some only the plasma ACTH values were high and beta-MSH values normal. No other anomalies of the corticotrophic and melanotrophic functions occurred in CAH as shown by the results of the provcative tests. Lastly, it must be emphasized that no modifications of plasma beta-MSH after synthetic MIF infusion were found in subject with normal or high plasma beta-MSH. These findings induce us to consider it unlikely that synthetic MIF is active in man.
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PMID:Corticotrophic and melanotrophic functions in congenital adrenal hyperplasia. 1 24

A wide range of doses was used to study the effect of Pro-Leu-Gly-NH2 (MIF) on the MSH release in rat pituitaries incubated in vitro. The Pro-Leu-Gly-NH2 was added to one half of the gland, and the other was used as control. The MSH released into the medium was measured by a bioassay and the activity of the samples referred to a standard of synthetic alpha-MSH. Pro-Leu-Gly-NH2 in doses of 10 to 30 ng/ml inhibited the MSH release in about 60%. Doses between 10(3) to 10(4) ng/ml induced neither release nor inhibition of the release of MSH. Dose of 10(5) ng/ml clearly induced release of MSH. The results of the additional experiments presented, although they represent no proof, are in line with the contention that Pro-Ley-Gly-NH2 in the natural MIF.
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PMID:New evidence that demonstrates that L-pro-L-leu-L-gly-NH2 might be the natural MIF. 3 62

The presence of alpha-MSH receptors on human melanoma has so far been suggested in the literature but not proved. We describe a reproducible and specific binding assay of alpha-MSH on human melanoma cells, using a high-specific-activity 125I-labelled hormone (1.5 to 2 mCi/micrograms) with consistent receptor binding (usually exceeding 2 pg/10(6) cells) and stable for 3 weeks. Asynchronized cells in suspension were incubated for 15 min at 37 degrees C with the tracer and various concentrations of unlabelled hormones. Synthetic alpha-MSH was compared to beta-MSH, ACTH1-24, ACTH4-10, beta-LPH, CLIP, CRF, MIF I, A8VP and beta-endorphin. Out of a panel of 8 human melanoma cell lines, 3 showed specific and reproducible alpha-MSH binding curves. No significant binding to human fibroblast and human carcinoma cells was seen. alpha-MSH, beta-MSH and, to a lesser extent ACTH4-10 (a part of the alpha-MSH sequence) were the only peptides able to displace labelled alpha-MSH from its binding sites, indicating the high specificity of the MSH receptor. Affinity constants (Ka) ranged from 10(8) to 10(9) l/mole and the estimated receptor number was 1,000 to 2,000 per cell. We conclude that some human melanoma cell lines expressed specific MSH receptors with stable affinity but which are low in number.
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PMID:Evidence for alpha-melanocyte-stimulating hormone (alpha-MSH) receptors on human malignant melanoma cells. 282 46

The neuropharmacological basis for d-amphetamine induced paradoxical behavioral thermoregulation remains unclear. This study examined thermoregulatory behavior of rats in a runway device that housed a heat source at one end and in which locomotion along the length of the runway could be observed. Sprague Dawley rats were pretreated with IP injections of saline, beta-endorphin, MIF-1, or alpha-MSH, with a repeat injection after 30 min. In a second experiment, d-amphetamine was administered as the repeat drug for all Ss. The results showed clear differences for heat-source-on vs. heat-source off. All peptides induced hypermotility, although no differentiated effects for the peptides on d-amphetamine induced paradoxical behavioral thermoregulation were found. These findings are discussed in light of the theoretical possibilities that: (a) a ceiling effect exists; (b) there are separate control systems for maintaining body temperature and another for behavioral thermoregulatory responses, and (c) other neurotransmitters may be involved in such induced paradoxical behavioral thermoregulation.
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PMID:The effects of MIF-I, beta-endorphin and alpha-MSH on d-amphetamine induced paradoxical behavioral thermoregulation: possible involvement of the dopaminergic system. 286 10

Developmental and long-term behavioral effects of perinatal injection of beta-endorphin (BE), CRF and Tyr-Pro-Leu-Gly-NH2 (Tyr-MIF-1) in male rats were investigated along with the possibility that opiate receptors may be altered by the injection of BE during this critical time. Daily injections of peptide were given to pregnant females (100 micrograms/rat) in the week before birth or to the offspring (50 micrograms/rat) of untreated mothers during the first week of life. Prenatal BE and CRF reduced body weight on day 1, in contrast to Tyr-MIF-1 which produced a significant increase over controls by day 7 as well as a slight but significant acceleration of eye opening. Among the postnatal treatments, CRF-treated animals showed the most dramatic changes. These included decreased body weight, accelerated eye opening, and, in adulthood, increased open field rearing behavior and a tendency for a monotonic body temperature response to low doses of morphine, in contrast to the biphasic response shown by controls. BE, when given to pregnant mothers, increased the number (Bmax) of [3H]naloxone-labeled (mu) receptors in whole brains of offspring assayed on day 14, but it did not significantly alter [3H]D-Ala-D-Leu-enkephalin-labeled (delta) receptors. In contrast, a significant decrease in both mu and delta receptors was observed on day 14 in rats given BE postnatally. These differences in receptors were no longer apparent in adulthood, and no significant differences in tail-flick response were detectable at this time. Nevertheless, some of the effects of these three peptides endured well beyond their presence, and for BE included changes in the number of opiate receptors.
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PMID:Developmental, behavioral, and opiate receptor changes after prenatal or postnatal beta-endorphin, CRF, or Tyr-MIF-1. 286 78

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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