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)

In this study, we investigated the hypothesis that increased opioid activity may be involved in the development of hyperinsulinemia in women with obesity and abdominal body fat distribution. Two groups of nine obese body (body mass index [BMI], 30 to 40 kg/m2) women with abdominal (A-ob) (waist to hip ratio [WHR] greater than 0.85) or gluteo-femoral (F-ob) (WHR greater than or equal to 0.80) fat distribution were examined and compared with eight normal-weight controls. Basal beta-endorphin levels were higher in the A-ob group than in the other groups. Each woman underwent two oral glucose tolerance tests (OGTT, 75 g glucose). A bolus of naloxone (0.8 mg) followed by a constant infusion of naloxone (0.04 mg/kg/h) or saline was also administered during the glucose challenge in random order, and blood samples for glucose, insulin, and C-peptide were collected at regular times after glucose administration. No difference was observed in basal or stimulated glucose concentrations between the three groups, nor between the saline or naloxone study. However, basal and stimulated insulin levels were significantly higher in obese women (particularly in the A-ob group) than in controls. Naloxone administration, however, did not significantly modify insulin and C-peptide glucose-stimulated concentrations in controls and in the F-ob group, whereas it significantly reduced (by approximately 47%) insulin levels in the A-ob group. Partial correlation coefficients showed a significant negative correlation between percent variation of glucose-stimulated insulin incremental areas during the naloxone study and the WHR in all women considered together (r = .544, P less than .025).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of the opioid peptides in the development of hyperinsulinemia in obese women with abdominal body fat distribution. 161 95

The effect of opioid neuropeptides was found to be more obvious in functional pathology of the higher nervous activity in hedgehogs. Met-enkephalin exerted a more obvious and longer-lasting effect on complicated forms of nervous activity, particularly inherent those. Naloxone abolished the met-enkephalin effect. The comparative effect of different opioid neuropeptides on inherent and acquired forms of nervous activity in mammals, the correlation between structural distribution of the neuropeptides and their functional properties, are discussed.
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PMID:[The effect of the opioid neuropeptides: met-enkephalin and beta-endorphin on the conditioned reflex activity of hedgehogs]. 166 69

In homogenate of rat olfactory bulb, the opioid receptor agonists beta-endorphin, Leu-enkephalin, and dynorphin A stimulated adenylate cyclase activity in a concentration-dependent manner, with half-maximal effects displayed at 22, 63, and 176 nM, respectively. The maximal stimulation of the enzyme activity corresponded to about a 40% increase of basal activity for all three peptides. Naloxone antagonized the stimulation of beta-endorphin, Leu-enkephalin, and dynorphin A, with pA2 values of 8.0, 7.7, and 8.1, respectively. Kinetic analysis performed with Leu-enkephalin showed that the opioid peptide increased the Vmax of the enzyme, without changing the Km for the substrate Mg-ATP. Moreover, the opioid stimulation was associated with a significant increase of the affinity of the enzyme for Mg2+ activation and occurred in membranes incubated in a Ca2(+)-free medium. Addition of exogenous GTP at micromolar concentrations was absolutely necessary for the detection of the opioid effect. Treatment of olfactory bulbs with cholera toxin did not alter the stimulation of adenylate cyclase by Leu-enkephalin. However, the opioid stimulation disappeared in membranes obtained from bulbs injected with pertussis toxin. These results demonstrate the presence in the brain of a new functional class of opiate receptors coupled to stimulation of adenylate cyclase via a transduction mechanism that is Ca2+ independent and seems to involve a pertussis toxin-sensitive GTP-binding protein.
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PMID:Naturally occurring opioid receptor agonists stimulate adenylate cyclase activity in rat olfactory bulb. 167 23

The electrically stimulated release of [3H]noradrenaline ([3H]NA) from slices of the nucleus tractus solitarii (NTS) from the rat in vitro was inhibited by the alpha 2-adrenoceptor agonist, clonidine, in a concentration-dependent manner and enhanced by the alpha 2-adrenoceptor antagonist, yohimbine. Phenylephrine, isoprenaline, carbachol, quinpirole and SKF 38393, all at 10(-6) M, did not affect the stimulus-evoked release of [3H]NA. The opioid peptides, alpha- and gamma-endorphin, did not have a significant effect on the stimulus-evoked release of [3H]NA; however, beta-endorphin reduced it in a concentration-dependent manner. [Leu5]Enkephalin also reduced [3H]NA release, but higher concentrations were necessary. The selective delta opioid receptor agonists, [D-Pen2,D-Pen5]enkephalin (DPDPE) and [D-Ser2(O-tert-butyl),Leu5]enkephalyl-Thr6 (DSTBULET), as well as the selective kappa opioid receptor agonist, U-69593, were not effective. The selective mu opioid receptor agonist, [D-Ala2,NMePhe4,Gly-ol5]enkephalin (DAGO), concentration dependently reduced the stimulus-evoked release of [3H]NA to the same extent as beta-endorphin did. Naloxone, while having no effect on stimulus-evoked [3H]NA release, antagonized the effect of DAGO. These results corroborate that the release of NA from noradrenergic terminals in the NTS region of the medulla oblongata of the rat is modulated via alpha 2-adrenoceptors and suggest that the release of NA in the NTS in rats is also modulated via mu opioid receptors.
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PMID:The electrically stimulated release of [3H]noradrenaline from nucleus tractus solitarii slices in vitro is modulated via mu-opioid receptors. 167 75

Naloxone and its congener, methyl naloxone, were given subcutaneously (s.c.) or centrally (i.c.v.) to 24-h water-deprived male rats 30 min prior to decapitation and the effect on plasma levels of vasopressin (VP) and oxytocin (OT) was studied. The potency of s.c. applied methyl naloxone to increase plasma OT levels did not differ from that of naloxone. Injected i.c.v., neither methyl naloxone nor naloxone had a clear effect and they antagonized i.c.v. co-administered dynorphin A-(1-13) equipotently. Methyl naloxone or naloxone, s.c., antagonized the inhibitory action of simultaneous dynorphin A-(1-13) and beta-endorphin-(1-31) given i.c.v., although higher doses of methyl naloxone were required. The data indicate that the sites of inhibition of neurohypophysial hormone release due to beta-endorphin-(1-31) are more likely to be located mostly within the blood-brain barrier, to which methyl naloxone has less ready access, than are the sites of inhibition due to dynorphin A-(1-13).
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PMID:Pharmacological assessment of the site of action of opioids on the release of vasopressin and oxytocin in the rat. 168 Jul 8

We have studied the effects of natural opioids on interleukin-1 (IL-1) -induced interleukin 2 (IL-2) production by the lymphoid cell line EL-4. beta-Endorphin (beta-end) significantly enhanced IL-2 production by IL-1-stimulated EL-4 cells. Similar results were obtained using the LBRM33-1A5 cell line. beta-End induced significant enhancement (35-100%) of IL-1-induced IL-2 production at all concentrations of IL-1 tested (2-0.25 U/ml) and the effects were seen with both IL-1 alpha and IL-1 beta. The dose response of beta-end augmentation of IL-1-induced IL-2 production was bimodal, with peak activities seen at high (10(-8)-10(-10) M) and low (10(-16) M) beta-end concentrations. The specificity of beta-end effect was studied using the opioid antagonist naloxone. Naloxone completely abolished the enhancing effects of beta-end, indicating that the effects might be mediated through binding to opioid receptors. In addition, other opioid peptides, including gamma-endorphin and enkephalins, elicited similar effects. Northern blotting analysis revealed higher levels of IL-2 mRNA in beta-end-treated IL-1-induced EL-4 cells than in IL-1-induced control cells. Thus, beta-end might enhance IL-2 production by either augmenting the transcription rate or increasing IL-2 mRNA stability. These results suggest that beta-end might play an important role in the regulation of lymphokine production in the periphery in addition to its known interactions with IL-1 in the central nervous system.
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PMID:Beta-endorphin modulation of IL-1-induced IL-2 production. 168 7

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

Morphine, leu-enkephalinamide, met-enkephalin, alpha-neoendorphin and its Arg8 1-8 fragment increase contractile vacuole output in the freshwater Amoeba proteus at 18 microM. Significant effects of leu-enkephalin and naloxone are obtained at 180 microM. All compounds have reached their maximal activity at 720 microM. Alpha-neoendorphin and leu-enkephalin are inactive in the presence of isotonic, non-penetration sucrose, hence these compounds increase plasma membrane permeability to water. Results from molecular modeling show a clear correlation of activity with amphiphilicity, charge distribution and general flexibility of molecules. We conclude that, like previously-studied vasopressin analogues and non-hormonal amphiphilic peptides, active opioids embed themselves into the Amoeba plasma membrane, disrupting the lipid bilayer and increasing its permeability. In our Amoeba system, naloxone, a general morphine-like inhibitor, blocks active opioids as well as a vasopressin analogue. Naloxone, being less active than other tested amphiphiles, acts as a membrane stabilizer, protecting the lipid bilayer against the disruption action of more active compounds.
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PMID:Direct membrane effects of morphine and endorphins on Amoeba proteus. 173 Nov 68

Brain neurons that express the pro-opiomelanocortin gene secrete multiple forms of beta-endorphin (beta E) which subserve diverse bioregulatory processes. beta E-1-31, for example, is a potent analgetic but beta E-1-27 acts as an opioid antagonist and beta E-1-26, as well as the N-acetyl derivatives of all 3 peptides, lack opioid receptor activity. The present study examines the effects of beta-endorphin processing on its central cardioregulatory potency. Consistent with previous reports, intracisternal beta E-1-31 (1.5 nmol) injection lowered mean arterial pressure (MAP); MAP was reduced by 29.7 +/- 3.9 mm Hg at 60 min and returned toward baseline by 120 min. Unexpectedly, beta E-1-27 displayed a 10-fold greater hypotensive potency than beta E-1-31. At 0.15 nmol, it produced a response equivalent to 1.5 nmol beta E-1-31 while 1.5 nmol beta E-1-27 sustained a maximal reduction in MAP (49.2 +/- 3.9 mm Hg) throughout the 120-min test period. In contrast, beta E-1-26 and N-acetyl-beta E-1-26, -1-27 and -1-31 were inactive at 1.5 nmol. Bradycardia accompanied the depressor response to the higher beta E-1-27 dose but not to beta E-1-31. Naloxone pretreatment completely blocked the depressor effects of both beta E-1-31 and beta E-1-27, and reversed the bradycardia produced by beta E-1-27, suggesting that both peptides act through opioid receptors. beta E-1-27 also stimulated catecholamine release from the perfused adrenal gland but beta E-1-31 was inactive. These findings emphasize the importance of regionally selected post-translational processing in defining the functional specificity of beta E peptides.
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PMID:Endoproteolytic conversion of beta-endorphin-1-31 to beta-endorphin-1-27 potentiates its central cardioregulatory activity. 188 2

To elucidate the mechanism of clonidine's effect on hormone release, serum growth hormone (GH), luteinizing hormone (LH), cortisol, and plasma beta-endorphin concentrations were determined after clonidine, naloxone, or the combined therapy of clonidine plus naloxone in six healthy women investigated in the luteal phase of their menstrual cycles. The clonidine injection increased GH levels. Naloxone (0.05, 0.1, and 0.2 mg/kg) decreased serum GH concentrations. Naloxone also increased serum LH, whereas clonidine decreased LH levels. Only the maximal dose of naloxone significantly increased serum cortisol concentrations. Clonidine had opposite effects on cortisol levels. These results demonstrate that combined therapy with clonidine plus naloxone leads to inhibition of the response of GH, LH, and cortisol to clonidine injection.
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PMID:The effect of clonidine on hormone release mediated through activation of opiate receptors. 196 78


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