Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

A combined dexamethasone-human corticotropin-releasing hormone (hCRH) test was applied to 63 individuals--44 patients with major depressive episode (22 male, age 49.5 +/- 13.4 years, and 22 female, 44.6 +/- 11.9 years) and 19 normal male controls (age 42.0 +/- 16.8 years). In normal controls, premedication with 1.5 mg dexamethasone at 11:00 PM substantially inhibited the stimulated release (expressed as area under the time course curve) of cortisol on the day after 100 micrograms hCRH was administered at 3:00 PM. In contrast, depressives responded with significant rises in cortisol (normal controls, 4.1 +/- 4.0 x 10(3) ng/ml/min; depressives, 12.7 +/- 8.3 x 10(3) ng/ml/min; p less than 0.01). Multiple stepwise regression analysis disclosed significant effects of age (T = 3.55, p less than 0.01) and severity of depression (T = 5.42, p less than 0.01) on cortisol release in patients. Such an influence of age upon pituitary-adrenocortical regulation was absent among healthy controls. We postulate that the underlying mechanisms involve changes in corticosteroid receptors in the brain of depressives, impairing the sensitivity with which the brain-pituitary system can detect the dexamethasone feedback signal. Altered glucocorticoid neuroregulation in depression is apparently accelerated by the aging process.
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PMID:Effect of age on the cortisol response to human corticotropin-releasing hormone in depressed patients pretreated with dexamethasone. 206 37

To explore and to compare hypothalamic-pituitary-somatotropic (HPS), hypothalamic-pituitary-thyroid (HPT) and hypothalamic-pituitary-adrenocortical (HPA) axis function in depression, 30 subjects (15 patients with a major depressive episode and individually matched controls) received 50 micrograms growth hormone-releasing hormone-44 amide at 9:00, 200 micrograms thyrotropin-releasing hormone (TRH) at 9:00 and 100 micrograms human corticotropin-releasing hormone (CRH) at 18:00 on consecutive days as an i.v. bolus dose. Compared with controls, depressed patients showed blunted growth hormone (GH) responses to GHRH, decreased TRH-induced thyrotropin (TSH) release and reduced corticotropin (ACTH) but normal cortisol secretion following CRH. ACTH secretion following CRH and TRH-induced TSH release were positively correlated across depressed patients and controls but no significant correlations between GH responses to GHRH and TRH-induced TSH release or ACTH and cortisol secretion following CRH administration were demonstrated. Our findings suggest that altered HPT and HPA axis function associated with depression are triggered by factors that are at least partly different from those that cause HPS system dysfunction. We conclude that the pathophysiological process resulting in aberrant neuroendocrine secretory dynamics associated with depression may primarily occur at a suprapituitary site, and that HPS, HPT and HPA axis dysfunction may be precipitated by complex central and peripheral regulatory mechanisms involving largely independent factors.
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PMID:Endocrine responses to growth hormone-releasing hormone, thyrotropin-releasing hormone and corticotropin-releasing hormone in depression. 254 70

Twenty subjects (10 patients with a major depressive episode and 10 individually matched healthy controls) received 100 micrograms synthetic human corticotropin-releasing hormone (hCRH) as an i.v. bolus dose. Healthy subjects and depressed patients exhibited a significant increase of plasma somatostatin (SRIH) concentrations with no difference between both comparison groups. Compared to controls, depressed patients showed a significant attenuation of corticotropin (ACTH) responses, while cortisol secretion in response to hCRH was normal. No correlations were found among basal plasma concentrations of SRIH, ACTH or cortisol and SRIH, ACTH or cortisol responses following hCRH. These findings are compatible with the hypothesis that hypothalamic-pituitary-adrenal (HPA) hyperactivity in the depressive state may primarily be due to central hypersecretion of CRH and support the view of a hCRH-induced SRIH secretion which is not related to HPA dysfunction associated with major depression.
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PMID:The influence of human corticotropin-releasing hormone on somatostatin secretion in depressed patients and controls. 256 52

The pathophysiology behind the abnormalities of the hypothalamic pituitary adrenal cortex axis found in patients with major depressive disorder was studied by the use of the vasopressin test. The response of plasma adrenocorticotropin (ACTH) and cortisol to the injection of 10 IU lysine-vasopressin (LVP) was investigated in 18 patients meeting the DSM-III criteria for major depressive episode. The response was correlated to the outcome of the dexamethasone suppression test (DST) with the use of two different cut-off points, 139 nmol/l and 200 nmol/l respectively. The results show that no significant difference was found in ACTH or cortisol response between patients having a normal or abnormal DST. The results do not seem to support the hypothesis that the abnormalities of the hypothalamic pituitary adrenal cortex axis involve a hypersecretion of corticotropin-releasing factor (CRF) and a subsequent desensitization of the corticotrophs to CRF-stimulated ACTH release.
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PMID:Adrenocorticotropin and cortisol response to lysine vasopressin in relation to the outcome of the dexamethasone suppression test in major depressive disorder. 283 10

The current concept that blunted adrenocorticotropic hormone (ACTH) response to human corticotropin-releasing-hormone (h-CRH) in depression is primarily determined by elevated circulating plasma cortisol levels is still unproven. We tested this hypothesis by comparing ACTH release following intravenous administration of 100 micrograms h-CRH in 10 normal controls and in 21 inpatients with a major depressive episode. Eleven of these depressed patients were pretreated with an oral dose of 2 g metyrapone, which inhibits cortisol biosynthesis by blocking C-11 beta-steroid-hydroxylase. This intervention deprives the entire system of cortisol, which is the major feedback signal for the regulation of ACTH secretion at various pituitary and limbic sites. ACTH responses, assessed as areas-under-time-course-curves, were: in normal controls, 6.8 +/- 2.4 (SD) pg/ml/min x 10(3); in unmedicated patients, 2.6 +/- 1.1 pg/ml/min x 10(3); and in metyrapone pretreated patients, 9.0 +/- 6.7 pg/ml/min x 10(3). Thus, ACTH release in unmedicated depressed patients was significantly (p less than 0.001, Mann-Whitney U-test) blunted when compared with normal controls. In contrast, this blunting was completely avoided after metyrapone pretreatment, which resulted in net ACTH responses that were indistinguishable from those of the controls.
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PMID:Blunting of ACTH response to human CRH in depressed patients is avoided by metyrapone pretreatment. 285 10

The authors measured pituitary adrenocortical responses to human corticotropin-releasing hormone (CRH) in 10 patients with a major depressive episode and 10 matched control subjects. Depressed patients had a significantly lower aldosterone and ACTH release, but cortisol and corticosterone responses were not different between groups.
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PMID:Blunted aldosterone and ACTH release after human CRH administration in depressed patients. 302 85

The possible hypersecretion involvement of corticotropin-releasing hormone (CRH) in the pathophysiology of hypothalamic-pituitary-adrenocortical axis disturbances in patients with major depressive episode and with an abnormal dexamethasone suppression test (DST) was investigated. The corticotropin (ACTH) and cortisol response to the injection of 45 micrograms of synthetic human CRH at 1630 were analyzed in 24 inpatients with normal (suppressors) or abnormal (nonsuppressors) DST. The outcome of the DST was analyzed using 3 cut-off points for the cortisol levels. The clinical assessments included two rating scales. The results showed that nonsuppressors had a significantly lower ACTH response to CRH stimulation than suppressors at all cut-off points (calculated as net area under the curve and as the difference between the peak and the baseline level) despite no significant differences in the severity of depression.
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PMID:Release of corticotropin after administration of corticotropin-releasing hormone in depressed patients in relation to the dexamethasone suppression test. 838 20

In an acute trial, three different dosages (60, 300, and 600 micrograms) of the endocrinologically inert but behaviorally active corticotropin 4-9 (ACTH4-9) fragment ebiratide were given to three patients with clinically probable Alzheimer's disease and five patients with a major depressive episode who were psychomotorly retarded. The drug was given intravenously in a double-blind, placebo-controlled, crossover design, and cognitive as well as psychopathologic assessments were carried out predrug and postdrug treatment. In summary, no adverse effect of the ACTH fragment was detected. In this explorative study, none of the patients improved cognitively, as measured by neuropsychologic testing. However, all patients, regardless of underlying disorder, reported a decrease of the feeling of tiredness or loss of energy, respectively. They felt more vigorous and alert. This occurred after any of the three doses of ACTH4-9, but not after placebo. In concert with reports from other studies, it is concluded that the ACTH4-9 fragment ebiratide may have activating properties in humans. However, given acutely, it does not seem to have antidementia or antidepressive efficacy.
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PMID:Behavioral effects of a synthetic corticotropin 4-9 analog in patients with depression and patients with Alzheimer's disease. 839 47

The neuroendocrine responses to subcutaneous (SC) administration of the dopamine (DA) agonist apomorphine (APO) hydrochloride (0.75 mg) were studied in a large group of subjects: 110 drug-free inpatients with either DSM-III-R schizophrenia (SCZ, n = 46), schizoaffective disorder (SAD, n = 14), or major depressive episode (MDE, n = 50), plus 18 hospitalized controls. Compared to a saline test, APO induced a significant increase of growth hormone (GH), adrenocorticotropin (ACTH), and cortisol (COR) release and a decrease in prolactin (PRL) secretion. No change in thyrotropin (TSH) levels was observed. In the total sample the extents of ACTH, COR and GH responses were correlated, but in the group of 88 subjects who exhibit a normal GH stimulation this correlation disappeared. This discrepancy suggests that APO-induced ACTH and COR stimulation may be mediated by pathways different from those mediating GH stimulation. According to diagnostical categories, we found significant lower ACTH and COR stimulation in the schizophrenic group and in patients with SAD, compared with that among controls or depressed patients. We found also a significant difference between subgroups of schizophrenic patients. These results agree with the hypothesis that different aspects of psychosis might involve different subtypes of DA-receptors with different localizations and sensitivities.
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PMID:Multihormonal responses to apomorphine in mental illness. 853 20

Altered negative feedback control of the hypothalamic-pituitary-adrenocortical (HPA) system is a frequent laboratory sign of major depression. It coincides with depressive episodes and partially reverses after recovery from psychopathology. Such an HPA disturbance in feedback control can be acquired as a result of stressful life experiences and be compounded by age or it can be genetically predetermined at all levels involved in fine-tuned neuroendocrine regulation. Major psychiatric disorders run in families and a high familial load for an affective illness therefore increases an individual's risk of becoming affected. We investigated whether the HPA feedback disturbance observed among patients with depression is present in otherwise healthy individuals who are at high risk for psychiatric disorders because they have a first-degree relative with an affective illness. Using rigid psychodiagnostic techniques, we screened 431 consecutively admitted patients with depression and identified 35 families with one or more high-risk probands (HRPs). The results of a combined dexamethasone/human corticotropin-releasing hormone (DEX-CRH) test showed that the group of dexamethasone-pretreated (1.5 mg; 23.00 h) HRPs released more cortisol after stimulation with human CRH (100 micrograms; 15.00 h the next day) than a control group (CPs), but less than a group of patients with an acute major depressive episode (DPs). The peak cortisol values were 146.1 +/- 147.7 nmol/l (mean +/- SD) (HRPs), 75.3 +/- 47.9 nmol/l (CPs) and 278.2 +/- 199.2 nmol/l (DPs), yielding significant (F = 9.66, p < 0.001) group differences, with values for HRPs vs. CPs and HRPs vs. DPs being significant at the 1% level (t test).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Altered hypothalamic-pituitary-adrenocortical regulation in healthy subjects at high familial risk for affective disorders. 854 47


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