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)

Carbamazepine, a tricyclic anticonvulsant with chemical resemblance to imipramine, has been recently successfully introduced as a prophylactic agent and acute treatment modality for manic-depressive illness (Ballenger and Post 1980; Okuma 1983; Post et al. 1984). The interest in carbamazepine emerges from its ability to dampen paroxysmal neuronal activity not only in epilepsy, but also in those particular systems that appear to be involved in the etiology of episodic affective illness (Post et al. 1983). These affective episodes are frequently associated with endocrine irregularities of the hypothalamic-pituitary-adrenocortical (HPA) axis, including increased cortisol secretion (Halbreich et al. 1985), nonsuppression of corticosteroids following dexamethasone, and blunted corticotropin (ACTH) release after stimulation with human corticotropin-releasing hormone (h-CRH) (Holsboer et al. 1986, 1987) or its heterologous ovine analog (Gold et al. 1986). Some recent reports have shown that carbamazepine treatment may interfere with HPA physiology, as it induces Dexamethasone Suppression Test (DST) nonsuppression (Privitera et al. 1982; Rubinow et al. 1984) and enhances mean urinary free cortisol secretion (Rubinow et al. 1986). To further explore the pathophysiology of this phenomenon of an altered HPA function, we conducted h-CRH tests in six patients in stable remission from major depression during long-term carbamazepine treatment to look for possibly drug-induced modulations. In two of six patients, we observed highly abnormal ACTH responses.
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PMID:Exaggerated corticotrophic cell response to human corticotropin-releasing hormone in two patients during long-term carbamazepine treatment. 284 Sep 79

Sera containing antibodies to beta-endorphin from 2 patients with major depressive disorder were shown to have antidiotypic antibodies that specifically inhibited reactivity between anti-beta-endorphin IgG and beta-endorphin. Autologous and homologous antiidiotypic anti-anti-beta-endorphin IgG antibodies were isolated by affinity chromatography. The purified antiidiotypic antibody did not bind beta-endorphin but competed with [125I]beta-endorphin for rat brain opiate receptors. Normal IgG that was similarly treated had negligible competitive effects. The antibody bound to the membrane preparation; such binding was inhibited by opiate receptor ligands. Binding of the antiidiotype to a 60,000-dalton protein from rat brain was detected by Western immunoblot analysis. This protein corresponds in molecular weight to proteins proposed to be components of opiate receptors. These findings imply that immune reactivity to neuropeptides could contribute to psychiatric impairment.
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PMID:Human antiidiotypic antibody against opiate receptors. 284 77

Human IgG specific for beta-endorphin was identified by enzyme-linked immunoabsorbent assay and isolated by affinity chromatography. From a sample of 27 subjects, three individuals with major depression demonstrated plasma IgG highly reactive with human beta-endorphin, while four other subjects (two with depression and two randomly selected blood donors) had intermediate reactivity. The recognition site for beta-endorphin was retained by F(ab')2 fragments.
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PMID:Anti-beta-endorphin immunoglobulin G in humans. 294 44

The hypothalamic-pituitary-adrenal (HPA) axis is dysregulated in many patients with depression, probably at all levels of the axis. To determine if HPA dysregulation is associated with severity of depression, we studied a group of 66 patients with major depressive disorder. Each patient underwent a pretreatment Dexamethasone Suppression Test, with plasma postdexamethasone cortisol determination at 8:00 AM, 4:00 PM, and 11:00 PM. All three postdexamethasone cortisol levels were significantly correlated with the Hamilton Rating Scale for Depression (HRSD) scores. We also examined the "profile" measures of mean, maximum, and minimum of the three cortisol values; again, all three were significantly correlated with HRSD scores. To evaluate associations between clinical severity and HPA dysregulation at the pituitary level, we studied a second group of 44 patients with major depressive disorder. Each had postdexamethasone cortisol determinations at 4:00 PM and 11:00 PM as well as pre- and postdexamethasone beta-endorphin determinations at 4:00 PM. The cortisol data from this group followed the same pattern as in the first sample, and there was a significant relationship between HRSD score and degree of beta-endorphin nonsuppression as well. These results suggest that severity of depression is one of the determinants of dysregulation at both adrenal and pituitary levels of the HPA axis, accounting for 10%-20% of the observed variance.
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PMID:Postdexamethasone plasma cortisol and beta-endorphin levels in depression: relationship to severity of illness. 295 96

The effect of a single dose (60 mg p.o.) of the serotonin agonistic agent fenfluramine (FNF) on plasma cortisol, prolactin (PRL), growth hormone (GH), and immunoreactive beta-endorphin (ir-beta-EP) levels was assessed in eight major depressed patients and eight controls. The hormones were monitored at basal level (0') and hourly during 5 h following FNF administration. The pharmacological challenge caused an elevation of 80% in PRL secretion in the healthy controls and only 42% in the depressed patients. However, the actual prolactin response (delta max) failed to discriminate depressed patients from controls. A blunted response followed by a decrease (33%) in serum cortisol levels was observed in depressed patients 5 h after drug administration while an increase of 94% was obtained in controls after 3 h. FNF provocation did not affect GH and ir-beta-EP plasma levels. The blunted cortisol responsiveness to FNF administration in depressed patients may reflect functional hypoactivity of central serotonergic system at least during the acute phase of major depression. It is not clear why the cortisol hyporesponsivity in depressed patients is not accompanied by a similar reduced PRL response to FNF challenge.
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PMID:Plasma cortisol, prolactin, growth hormone, and immunoreactive beta-endorphin response to fenfluramine challenge in depressed patients. 296 72

Synthetic ovine corticotropin releasing factor (o-CRF) was administered as an intravenous bolus (100 micrograms) to eight patients suffering from a major depressive disorder, endogenous subtype. All patients showed inadequately suppressed cortisol levels after 1 mg dexamethasone. After clinical remission and normalized dexamethasone responses, these patients were reinvestigated with o-CRF stimulation. The mean adrenocorticotropic hormone (ACTH) release from the pituitary corticotroph cells was indiscriminate at both test sessions. Cortisol and corticosterone output after o-CRF tended to be higher during depression than after recovery. The o-CRF-induced increments observed with corticosterone were more marked in comparison with cortisol. Within the limitations of the current protocol, our preliminary data lend support to the view that an increased pituitary ACTH reserve or adrenocortical steroid reserve is not likely to be responsible for the defective pituitary-adrenal regulation in some dexamethasone-resistant depressives.
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PMID:ACTH, cortisol, and corticosterone output after ovine corticotropin-releasing factor challenge during depression and after recovery. 298 88

Efforts to elucidate the abnormal mechanism of corticotropin and beta-endorphin in major depression have yielded conflicting findings. The relationship of plasma levels of cortisol, corticotropin, and beta-endorphin in 42 patients with a Research Diagnostic Criteria diagnosis of major depression, endogenous subtype was examined. Following the DST, 32 patients were nonsuppressors and 10 were suppressors. The differences between the median values for plasma corticotropin and beta-endorphin immunoreactivity were not significant at any time of measurement after the DST.
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PMID:Plasma levels of cortisol, corticotropin, and beta-endorphin in patients with major depression. 301 93

To measure opiate receptor sensitivity, the effects of naloxone on beta-endorphin and cortisol serum levels were determined before and after 3 weeks of clomipramine treatment (75 mg/day i.v.) in 12 patients with major depressive disorder. The opiate antagonist significantly increased both hormonal levels. The only significant endocrine differences between pre- and post-treatment were basal and maximal cortisol levels, which were elevated before antidepressant therapy. The rise in the cortisol or beta-endorphin serum level after naloxone injection was not affected by clomipramine treatment. There was no significant relationship between depression score and basal or stimulated endocrine variables. These data do not indicate a distinct effect of antidepressants on opiate receptor sensitivity.
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PMID:Opiate receptor sensitivity in depressed patients before and after clomipramine treatment. 302 Jan 8

ACTH alpha 1-24 (cosyntropin) (250 micrograms by intravenous bolus) was given to 38 medicated patients with major depressive disorder (MDD) and to 34 normal control subjects. Patients with MDD had significantly higher plasma cortisol concentrations and significantly higher increases in plasma cortisol levels 60 minutes after cosyntropin infusion than did control subjects. Patients who were nonsuppressors in the dexamethasone suppression test had significantly higher 60-minute cortisol concentrations and cortisol increases than did normal subjects and patients with MDD who were suppressors. There were significant, strongly positive correlations between cortisol secretory responses to cosyntropin and postdexamethasone cortisol concentrations in patients with MDD. These findings confirm that adrenal sensitivity to corticotropin (ACTH) is enhanced in MDD and suggest that this endocrine abnormality may be related pathophysiologically to the resistance of cortisol secretion to dexamethasone suppression.
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PMID:Enhanced adrenal sensitivity to exogenous cosyntropin (ACTH alpha 1-24) stimulation in major depression. Relationship to dexamethasone suppression test results. 303 Feb 18

Cerebrospinal fluid (CSF) levels of beta-endorphin (beta-EP) were measured in 9 migraineurs with interparoxysmal headache (MIH), in 13 patients with major depression in an active phase (5 suffered from MIH), and in 16 age-matched controls. beta-EP was measured by specific RIA after gel-chromatography. While beta-EP levels of depressed patients (58.5 +/- 21.0 fmol/ml, M +/- SD) were similar to those of controls (65.8 +/- 26.6), those of migraineurs (15.0 +/- 11.1) were significantly reduced (p less than 0.01). In depressed patients also suffering from MIH, beta-EP concentrations (22.8 +/- 7.2, p less than 0.05) were half those reported in depressed patients without pain problems. The reduced CSF beta-EP levels in patients whose headache and depression coexist support the notion that this neuropeptide is concerned with chronic pain, independently of the affective state.
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PMID:CSF beta-EP in headache and depression. 316 Apr 71


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