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)

Mineralocorticoid function of the adrenal cortex and the activity of the renin-angiotensin system were studied in patients with Itsenko-Cushing's disease before (36 cases) and after (27 cases) the treatment with chloditan--an adrenocortical inhibitor. Minertalocorticoid function of the adrenal cortex was assessed by the blood immunoreactive aldosterone content, urinary 18-aldosterone-glucuronide excretion, and the rate of aldosterone secretion. Condition of the renin-angiotensin system was assesed by the blood renin activity. Aldosterone and renin concentration was studied by the radioimmunological method. There proved to be a reverse relationship between the blood aldosterone concentraiton and the severity of Itsenko-Cushing's disease. Elevation of the mineralocorticoid function of the adrenal cortex in Itsenko-Cushing's disease was due to activation of the renin angiotensin system. During clinical remission of the disease following a course of chloditan treatment the patient displayed an increased blood aldosterone level and a rise of its secretion. The minralocorticoid function of the adrenal cortex was intensified at the state of clinical remission because of an increased blood corticotropin concentration.
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PMID:[Mineralocorticoid function of the adrenal cortex and the renin--angiotensin system in Itsenko-Cushing's disease]. 70 55

The adrenocorticotropic hormone (ACTH), cortisol, and growth hormone responses to four consecutive, logarithmically increasing doses of intravenous diazepam compared with placebo given at 15-min intervals were examined in patients with panic disorder (n = 13), generalized anxiety disorder (n = 8), and healthy controls (n = 13). Diazepam caused dose-dependent decreases in cortisol and increases in GH and dose-independent decreases in ACTH. There were no patient-control differences, possibly due to either the small sample size of the experimental paradigm, which tested subjects in an upright, sitting position in mildly arousing circumstances.
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PMID:Neuroendocrine effects of diazepam in panic and generalized anxiety disorders. 165 36

The rate-limiting step in the biosynthesis of steroids is the transport of the substrate cholesterol from the outer to the inner mitochondrial membrane, where cholesterol is metabolized to pregnenolone. This transport is markedly stimulated by the action of hormones, such as adrenocorticotropic hormone (ACTH) and luteinizing hormone (LH) for adrenocortical and testicular Leydig cells, respectively. Recently, it was demonstrated that the peripheral-type or mitochondrial benzodiazepine receptor, abundant in steroidogenic tissues, is involved in the regulation of steroid biosynthesis. In search for an endogenous ligand for mitochondrial benzodiazepine receptors, regulating steroidogenesis, the effects of Diazepam Binding Inhibitor (DBI) were studied. The model systems used were the Y-1 adrenocortical and the MA-10 Leydig cell lines, previously shown to be valid steroidogenic models. Both cell lines contain significant levels of immunoreactive DBI. Purified DBI from rat brain, at high nanomolar concentrations, increased formation of pregnenolone, when added to mitochondrial preparations of both cell types; but at concentrations of DBI above 1 microM, a decrease in the stimulation was observed. Flunitrazepam, a benzodiazepine which binds to mitochondrial benzodiazepine receptors, with high nanomolar affinity, inhibited the stimulatory action of DBI on the formation of mitochondrial pregnenolone, indicating that DBI exerts its stimulatory effects through an action on mitochondrial benzodiazepine receptors. In order to determine the biologically active amino acid sequence in the DBI molecule, various fragments of DBI were synthesized and tested; also, peptides structurally unrelated to DBI were tested.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of diazepam binding inhibitor and its processing products at mitochondrial benzodiazepine receptors: regulation of steroid biosynthesis. 166 68

Diazepam binding inhibitor (DBI) is a neuromodulatory peptide for gamma-aminobutyric acid (GABA) neurotransmission. Levels of DBI in cerebrospinal fluid (CSF) were found to be elevated in depressed patients, when compared to age- and sex-matched normal controls. Levels of the peptide, corticotropin-releasing hormone (CRH), in CSF have been found to be elevated in depressed patients. Significant positive correlations between levels of DBI and CRH in the CSF of depressed patients and normal controls were found. These data suggest the possibility that DBI may have a role in coordinating responses to stress in humans, in addition to its possible role in the pathophysiology of depression.
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PMID:Cerebrospinal fluid diazepam binding inhibitor in depressed patients and normal controls. 178 40

Diazepam-binding-inhibitor (DBI) and gamma-aminobutyric acid (GABA) are colocalized in neurons in the brain. This system has been implicated in anxiety and in the regulation of corticotropin-releasing hormone (CRH) secretion. Alcohol has direct and indirect effects on the functioning of GABAA receptors. Abstinent alcoholics are, on the average, more anxious than controls. In tests of animal behavior, DBI has anxiogenic, and alcohol has anxiolytic potency. Therefore, we compared alcoholic patients and healthy controls for cerebrospinal fluid (CSF) levels of DBI, and looked for a correlation between CSF levels of DBI and CRH. There was no significant difference in CSF concentrations of DBI between the two groups and no significant correlation between CSF DBI and our measure of anxiety. However, there was a significant positive correlation between CSF levels of DBI and CRH in both the alcoholic and control groups.
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PMID:CSF diazepam-binding inhibitor in alcoholics and normal controls. 233 58

Rats were trained and tested in a step-down inhibitory avoidance task (0.3-mA footshock). Training-test interval was 6 h. In Experiment 1, animals received, 1 h before training, an ip injection of vehicle or diazepam (2.0 mg/kg) and, 30 s after training and/or 30 min prior to testing, ip saline, epinephrine (6.25 micrograms/kg or 125.0 micrograms/kg), naloxone (0.5 mg/kg), or beta-endorphin (1 micrograms/kg). In the vehicle-pretreated animals, post-training epinephrine (6.25 micrograms/kg) and naloxone enhanced, and post-training beta-endorphin and epinephrine (125.0 micrograms/kg) reduced, retention test performance; and pretest beta-endorphin and epinephrine (125.0 micrograms/kg) reversed the latter effect and enhanced retention on their own. Diazepam lowered memory scores on its own and prevented all other drug effects with the exception of post-training facilitation by epinephrine (6.25 micrograms/kg). In previous papers it was shown that post-training facilitation by epinephrine is due to an influence on storage processes, whereas all the other drug effects described above result from the post-training establishment of state dependency to either beta-endorphin or epinephrine, and therefore to a process involving further acquisition and storage. The present findings suggest that diazepam selectively hindered the acquisition and/or storage processes involved in state dependency. This conclusion is strengthened by the findings from Experiment 2, which showed, using a classic 2 x 2 design, that diazepam itself did not induce state dependency but, rather, depressed acquisition and/or storage of the avoidance task.
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PMID:Diazepam prevents post-training drug effects related to state dependency, but not post-training memory facilitation by epinephrine. 252 17

Plasma beta-endorphin, pain and anxiety were measured in patients before, during, and 1 and 3 hours following oral surgery. Diazepam and fentanyl blocked the stress induced increase in plasma beta-endorphin experienced by patients administered placebo. Moreover, intra-operative anxiety and post-operative pain appear to constitute independent and possibly equipotent stimuli for release of pituitary beta-endorphin in humans.
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PMID:Plasma beta-endorphin levels in oral surgery patients following diazepam, fentanyl or placebo. 608 14

Diazepam-induced feeding in rats is antagonized not only by the opiate antagonist naloxone but also intraventricular administration of specific antisera to the endogenous opioid peptides met-enkephalin or beta-endorphin. Pituitary beta-endorphin is probably not implicated in the diazepam effect since blockade with the glucocorticoid dexamethasone of the release of beta-endorphin from the anterior pituitary does not modify the diazepam-induced feeding, which is however prevented by TRH, a suggested physiological antagonist of some of the effects of opioid peptides. The possible central participation of both beta-endorphin and met-enkephalin in the ingestive behavior induced by diazepam gives further support to the postulated physiological role of endogenous opioids in appetite regulation.
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PMID:Antagonism of diazepam-induced feeding in rats by antisera to opioid peptides. 609 Aug 35

Six patients with Nelson's syndrome were given sodium valproate with or without diazepam for 3 or 5 weeks. Initial high plasma adrenocorticotropic hormone (ACTH) concentrations were greatly reduced by treatment and returned to high levels when treatment was stopped. Diazepam did not add significantly to the effects of sodium valproate alone. Three patients reported a decrease in the severity and frequency of headaches while on sodium valproate. In five patients abnormal skin pigmentation was reduced. Sodium valproate is a gamma-aminobutyric acid (GABA) transaminase inhibitor and it is suggested that the drug raises GABA levels in the hypothalamus and that this is responsible for the reduction in ACTH secretion. The data are consistent with the hypothesis that Nelson's syndrome is a neuroendocrine disease caused by a deficiency in the hypothalamic GABA-ergic system.
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PMID:Effect of treatment with sodium valproate and diazepam on plasma corticotropin in Nelson's syndrome. 611 28

Diazepam inhibits morphine tolerance and dependence and reverses a decrease in the met-enkephalin level in brain induced by morphine. In this study, we investigated whether inhibition of morphine-induced tolerance and dependence by diazepam involved a change in cyclic AMP levels in discrete rat brain regions and spinal cord. Male Sprague-Dawley rats were made tolerant and dependent by subcutaneous (s.c.) implantation of six morphine pellets (two pellets on the first day, and four on the second day). Diazepam (0.25 mg/kg b. wt) was injected once daily intraperitoneally (i.p.) for 5 days. Control rats were implanted with placebo pellets and injected once daily with saline or diazepam (i.p.). Tail-flick antinociception was measured 1 h after injections everyday. Animals were administered s.c. naloxone (10 mg/kg) to induce naloxone-precipitated withdrawal syndrome on the final day of the experiment (day 5), and the jumping behavior was observed for 30 min. Concomitant treatment with diazepam (0.25 mg/kg) significantly decreased the development of morphine tolerance and dependence. Diazepam (0.25 mg/kg) treated rats also showed a significant decrease in the jumping behavior compared to animals treated with morphine alone. Rats were sacrificed 2 h after the injection of saline or diazepam (0.25 mg/kg) on the fifth day. Cyclic AMP was estimated by RIA. In the control rats, the concentration of cyclic AMP in cortex was > hippocampus > cerebellum > hypothalamus > striatum > midbrain > pituitary > pons/medulla > spinal cord. There was no change in the concentration of cyclic AMP in any of the brain regions examined from morphine tolerant animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of morphine tolerance and dependence by diazepam and its relation to cyclic AMP levels in discrete rat brain regions and spinal cord. 779 44


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