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)

N-pro-opiomelanocortin (N-POMC) is secreted from the same precursor as ACTH and beta-endorphin. Elevated plasma ACTH and beta-endorphin/beta-lipotrophin concentrations have been reported in depression, however there have been no previous studies of N-POMC. Twenty-five patients with major depression and 18 control subjects were studied at five timepoints to examine diurnal rhythm and the effect of a dexamethasone suppression test. N-POMC was measured using a newly developed two-site recognition immunoradiometric assay (IRMA). This demonstrated advantages of sensitivity, specificity and simplicity compared with existing radioimmunoassays. N-POMC exhibited a pattern of diurnal rhythm and suppression in response to dexamethasone as described for other POMC derived peptides. Depressed subjects had higher levels of N-POMC at 0900 h post-dexamethasone than did control subjects. In conclusion, the results of this study are consistent with a hypothesis of cosecretion of POMC-derived peptides. N-POMC has a similar pattern of abnormal concentrations to ACTH and beta-endorphin/beta-lipotrophin in depression. This constitutes probable evidence of POMC-derived peptide resistance to glucocorticoid feedback in this condition.
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PMID:A multiple timepoint study of N-terminal pro-opiomelanocortin in depression using a two-site recognition immunoradiometric assay. 316 5

To explore changes in immune cell status with changes in the hypothalamic-pituitary (HP) axis in 20 patients with major depression as compared with 20 age-, sex-, and race-matched control subjects, we examined peripheral blood mononuclear cells (PBMC) for total T-cells (T3), total B-cells (B1), two T-cell subsets (T4 and T8), and natural killer cells (NKH1), and we measured the plasma level of cortisol, adrenocorticotropic hormone (ACTH), growth hormone (GH), and prolactin (PRL). The ratio of T4/T8 was increased in the patients. Within the group of control subjects only, increasing age correlated significantly with decreasing plasma PRL. Within the group of patients only, GH positively correlated significantly with T8 and NKH1, as did PRL with NKH1. No between-groups difference was found for T3, B1, T4, T8, NKH1, cortisol, ACTH, GH, or PRL.
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PMID:Immune cells and the hypothalamic-pituitary axis in major depression. 326 80

It is well established that corticotropin-releasing factor (CRF), a peptide comprised of 41 amino acids, is the major physiological regulator of the pituitary-adrenal axis by virtue of its role as the hypothalamic hypophysiotropic hormone that modulates the secretion of adrenocorticotropin (ACTH) from the anterior pituitary gland. In addition to its neuroendocrine role, CRF appears to function as a neurotransmitter or neuromodulator in extrahypothalamic brain areas. The peptide and its receptors are distributed throughout the central nervous system (CNS), and CRF is released by depolarizing concentrations of potassium in a calcium-dependent manner. After direct CNS administration, CRF produces a number of behavioral and physiological effects that are reminiscent of both an organism's response to stress and to the symptoms of patients with major depression. These include: diminished food consumption, decreased sexual behavior, disturbed sleep, alterations in locomotor activity and sympathetic nervous system activation. Alterations in regional brain CRF concentration in rats were observed after acute and chronic stress, i.e. decreased hypothalamic and increased locus coeruleus CRF concentrations. To test the hypothesis that CRF is hypersecreted in patients with major depression, the concentration of CRF in cerebrospinal fluid (CSF) in drug-free depressed patients and age- and sex-matched controles was measured in two studies. The depressed patients exhibited a clear group-related increase in CSF CRF concentrations. To further test this hypothesis that CRF is chronically hypersecreted in depressed patients, the number and affinity of CRF receptors in frontal cortex was measured in a group of suicides and age-matched controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of corticotropin-releasing factor in the pathogenesis of major depression. 329 91

The effect of acute and subchronic acrylamide treatment on levels of dopamine, serotonin, and their metabolites was determined in several brain regions of the rat. Concentrations of several neuropeptides and circulating hormones were also measured. Both a single and repeated doses of acrylamide resulted in elevated levels of 5-hydroxyindolacetic acid in all regions studied (frontal cortex, striatum, hippocampus, brain stem, and hypothalamus). Changes in regional content of other monoamines were much less pronounced. Turnover studies following pargyline blockage of monoamine oxidase, suggested results were due to increased rates of serotonin turnover in acrylamide-treated rats. Changes in neuropeptide levels were only detected in the hypothalamus where a single acrylamide treatment caused elevated levels of beta-endorphin and substance P, and in frontal cortex where met-enkephalin levels were higher after repeated acrylamide injection. Such repeated injection caused a major depression in plasma levels of testosterone and prolactin.
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PMID:Effect of acrylamide on neurotransmitter metabolism and neuropeptide levels in several brain regions and upon circulating hormones. 618 40

Immunoreactive (ir) plasma beta-endorphin level was assayed in ten symptomatic patients with a unipolar major depressive disorder and in 16 psychiatrically normal controls matched for age and sex. Plasma ir-beta-endorphin level in depressed patients was similar to that in controls. All depressed patients was similar to that in controls. All depressed patients had a transient, approximately threefold increase in ir-beta-endorphin after each use of electroconvulsive therapy (ECT). The increase of plasma ir-beta-endorphin level after ECT parallels the transient elevation of adrenocorticotropic hormone level reported by others and probably reflects a hypothalamic response to ECT.
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PMID:Plasma immunoreactive beta-endorphin levels in depression. Effect of electroconvulsive therapy. 629 23

Disturbances of hypothalamic-pituitary-adrenal regulation are frequently observed in a subgroup of patients suffering from major depression. The mechanism of hypothesized pituitary and hypothalamic involvement in this dysregulation remains relatively uncharacterized. In this paper we investigated the response of adrenocorticotropin (ACTH), as well as cortisol, to dexamethasone inhibition and characterized the dynamic response of ACTH to a one-hour infusion of cortisol in normal subjects and patients suffering from depression. A paradoxical increase in ACTH in response to cortisol is noted in one patient.
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PMID:Regulation of ACTH and cortisol in depression. 631 7

Sixteen patients with major depressive disorder who were nonsuppressors on the dexamethasone suppression test (DST) on hospital admission were studied for plasma levels of adrenocorticotropic hormone (ACTH). Eight patients reverted to normal suppression with clinical recovery, while eight remained nonsuppressors. There was a significant reduction of ACTH levels in those who normalized on their DST, while ACTH levels remained high in the group that continued to be nonsuppressors. The results favored the hypothesis that dexamethasone nonsuppression in depression is mediated by high ACTH levels.
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PMID:Plasma ACTH levels in depression before and after recovery: relationship to the dexamethasone suppression test. 632 Feb 45

Plasma cortisol levels of 28 hospitalized patients meeting Research Diagnostic Criteria for major or nonmajor (minor or intermittent) depression were significantly higher than those of eight normal subjects. In contrast, plasma beta-endorphin immunoreactivity was significantly lower in patients with nonmajor depression than in those with major depression or in normal subjects. A low ratio of plasma beta-endorphin to cortisol immunoreactivity was found to characterize patients in both groups. Through the use of only this ratio, a post-hoc analysis identified 25 depressed patients and seven controls. These findings have implications for psychiatric diagnosis and the involvement of the endogenous opioid system in the pathogenesis of depression.
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PMID:Plasma cortisol and beta-endorphin immunoreactivity in nonmajor and major depression. 632 98

Alterations in the hypothalamic-pituitary-adrenal (HPA) system are well documented in affective disorders. In depression these include increased secretion of cortisol, an insufficient suppressibility of cortisol by dexamethasone, a blunted corticotropin (ACTH) response to corticotropin-releasing hormone (CRH) and a dysfunction of the glucocorticoid receptor. Patients with atopic eczema, a common chronic skin disease, show seasonal variations in disease activity, symptoms of minor depression and immunological disturbances similar to those seen in patients with depression. To explore the integrity of the HPA system integrity in individuals with atopic eczema we studied the 24-h cortisol secretion and the cortisol, ACTH and beta-endorphin responses to CRH in such individuals and in healthy controls matched for sex and age. The 24-h secretion of cortisol did not differ between the patients with atopic eczema and the controls. The net response to CRH administered as a 100 micrograms i.v. bolus was significantly attenuated for both cortisol (24,235 +/- 12,443 vs. 47,019 +/- 34,515 nmol.min/dl; p < .03) and for ACTH (546 +/- 205 vs. 727 +/- 310 pmol.min/l; p < .05) in the patient group, whereas the beta-endorphin response did not differ between the groups (1072 +/- 448 vs. 1603 +/- 421 nmol.min/l). The blunted response of cortisol and ACTH cannot be explained by hypercortisolism as it is the case in major depression. Rather, it may be related to a prolonged underexposure to hypothalamic CRH or to an increased sensitivity of glucocorticoid feedback inhibition.
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PMID:Cortisol, corticotropin, and beta-endorphin responses to corticotropin-releasing hormone in patients with atopic eczema. 767 38

Recently, renewed interest has developed in the concept of anxious depression. Using an operational definition of "anxious depression" based on the SADS interview, 25 patients with major depressive disorder were separated into anxious (n = 14) and nonanxious (n = 11) subtypes. These two patient groups and normal control subjects received an intravenous corticotropin-releasing hormone challenge test. Adrenocorticotropic hormone (ACTH) and cortisol responses were compared among the three groups. Patients with anxious depression had significant attenuation of ACTH response when compared to nonanxious patients and normal control subjects.
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PMID:CRH challenge test in anxious depression. 777 46


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