Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Baseline beta-endorphin and cortisol levels and their responses to 1 mg dexamethasone were measured in 11 healthy controls and in 35 depressed patients, categorized according to the DSM-III. Dexamethasone significantly suppressed beta-endorphin levels. Depressed patients with melancholia/psychotic features exhibited significantly increased post-dexamethasone beta-endorphin levels compared with healthy controls, minor and simple major depressives; the baseline beta-endorphin levels did not differ between those study samples. Post-dexamethasone beta-endorphin and cortisol values were found to be significantly and positively correlated. Accordingly, cortisol non-suppressors showed significantly higher post-dexamethasone beta-endorphin levels. Post-dexamethasone beta-endorphin may be the most sensitive and specific reflection of the disorder in negative feedback exerted by dexamethasone in depression.
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PMID:An augmented escape of beta-endorphins to suppression by dexamethasone in severely depressed patients. 213 59

Studies in depression using a maximal stimulatory dose of corticotropin releasing factor have concluded that elevated resting cortisol levels in depressed patients exert a negative feedback effect on the corticotroph, resulting in a decreased corticotropin response. In this preliminary report, we examine the effects of a submaximal dose of corticotropin releasing factor on the release of another corticotroph secretory product, beta-lipotropin-beta-endorphin. We observed a decreased beta-lipotropin-beta-endorphin response in depressed subjects, but a normal adrenal cortisol response. Although the total beta-lipotropin-beta-endorphin response was decreased, the initial secretory response did not differ between patients and normal controls. Rather, the patients appeared to turn off secretion faster. This rapid shutoff was seen in all patients regardless of resting cortisol levels, suggesting that resting cortisol levels alone do not explain the decreased response seen in depressed patients.
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PMID:Beta-lipotropin-beta-endorphin response to low-dose ovine corticotropin releasing factor in endogenous depression. Preliminary studies. 213 63

L-5-Hydroxytryptophan (5HTP) was administered to 20 patients suffering from panic disorder and to 20 healthy controls. Subjects received 60 mg 5HTP in 300 ml saline solution. Before, during, and up to 2 hours after 5HTP administration, symptoms of anxiety and depression were assessed. In addition, plasma 5HTP, 3-methoxy-4-hydroxyethylglycol (MHPG), cortisol, beta-endorphin, and melatonin levels were measured at several time points, and the kinetics of 5-hydroxytryptamine (5HT) in blood platelets were measured. During and after the infusion of 5HTP, none of the patients showed an increase in anxiety or depressive symptoms, despite the presence of severe side effects. Some patients even experienced the 5HTP infusion as a relief. In contrast to the patients, nine control subjects reported depressed mood, although no increases in anxiety were noted. In both patients and controls, the 5HTP infusion led to substantial increases in plasma cortisol and beta-endorphin levels, while the plasma MHPG level was unchanged. Plasma melatonin increased significantly after 5HTP administration, suggesting that increasing 5HT availability in man might affect melatonin synthesis. The results of this study are at odds with the hypothesis that there is a supersensitivity of 5HT2 receptors in panic disorder.
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PMID:Behavioral, neuroendocrine, and biochemical effects of 5-hydroxytryptophan administration in panic disorder. 213 31

Circulating levels of cortisol and beta-endorphin were evaluated in basal condition and following dexamethasone administration in 20 healthy subjects and in 60 subjects suffering from hyperphagic obesity. Moreover, mental tests were administered to these subjects in order to evaluate the affective state. Our data showed that in obese patients B-Ep plasma levels were significantly higher than those of the control group, while cortisol plasma levels were similar in the two groups. Dexamethasone administration decreased cortisol plasma levels in normal and obese subjects, while did not modify B-Ep plasma levels in obese subjects. However, after dexamethasone administration 16.6% of the obese subjects did not show a complete decrease of cortisol level. This group of subjects obtained the highest scores for depression and hypochondria to MMPI.
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PMID:[Neuroendocrine changes and affective disorders in patients with hyperphagic obesity]. 214 22

The dexamethasone suppression test (DST) has been suggested as an effective tool for differentiating between depression and dementia. After administering 1 mg dexamethasone, we measured cortisol, ACTH, and beta-endorphin levels in 32 nondepressed patients with idiopathic Parkinson's disease (PD) (14 also with dementia) and 20 healthy, age-matched controls. Four of the 20 controls, 9 of the 18 with PD alone, and 8 of the 14 with PD and dementia were dexamethasone nonsuppressors (cortisol value greater than or equal to 5 micrograms/100 ml). PD patients without dementia (nonsuppressors) showed higher basal plasma values of cortisol (22.06 +/- 5.30 micrograms/100 ml) compared with the suppressors (13.38 +/- 3.30 micrograms/100 ml). Plasma ACTH and beta-endorphin responded in a coupled way to dexamethasone challenge. Higher basal levels of both peptides were found among PD patients (demented and nondemented), nonresponders to DST. Thus, the DST does not appear to be effective in differentiating between depression and dementia in PD. In addition, PD nonsuppressors showed higher basal values of plasma ACTH, beta-endorphin, and cortisol (similar to patients with major depression). This suggests that although the depression is clinically undetectable, both disorders may share some pathophysiological features at the hypothalamic hypophyseal adrenal level.
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PMID:Cortisol, ACTH, and beta-endorphin after dexamethasone administration in Parkinson's dementia. 215 5

There is current controversy over the mechanisms underlying hypothalamic-pituitary-adrenal (HPA) axis hyperactivity in depression. Pro-gamma-melanocyte-stimulating hormone (MSH), a portion of the N-terminal region of pro-opiomelanocortin, has been shown to act synergistically with adrenocorticotropic hormone (ACTH) in stimulating corticosteroid secretion both in vitro and in vivo. Pro-gamma-MSH and ACTH plasma levels were measured in 30 drug-free male patients with a DSM-IIIR major depressive disorder and 21 healthy controls. The baseline levels were similar in the two groups. After single-dose metyrapone stimulation, both hormones increased, but pro-gamma-MSH was significantly higher in control subjects than in depressives. After overnight 1-mg dexamethasone, ACTH was significantly less suppressed in depressives than controls. These results suggest that HPA axis dysregulation in depression may involve peptides other than ACTH and be more complex than previously reported.
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PMID:Effects of metyrapone and dexamethasone upon pro-gamma-MSH plasma levels in depressed patients and healthy controls. 217 Apr 84

Previous research in neuroendocrinology has evidenced that hyperactivity of the hypothalamic-pituitary-adrenal axis (HPA) depends on hypersecretion of corticotropin-releasing hormone (CRH). The aim of this study was to investigate the activity of HPA before and after recovery in depressed patients treated with electroconvulsive therapy (ECT). An h-CRH-stimulation test was performed on 2 occasions with examination of the HPA axis before ECT treatment during episodes of major depressive disorders with melancholia, and during the recovery phase after treatment. The results showed that patients during depression had significantly higher plasma levels of cortisol at 15 and 30 min after h-CRH-administration than after recovery. Depressed patients had significantly higher plasma levels of beta-endorphin 30 min after h-CRH-stimulation. The results are in agreement with previous studies, which have shown hypercortisolemia during depression. A possible hypersecretion of CRH may explain the effect on cortisol and beta-endorphin. No significant differences were found between cumulative responses of corticotropin, cortisol and beta-endorphin, calculated as the areas under the concentration curves.
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PMID:Corticotropin, cortisol and beta-endorphin responses to the human corticotropin-releasing hormone during melancholia and after unilateral electroconvulsive therapy. 185 69

1. The plasma levels of L-tryptophan (L-TRP) and the sum of five competing amino acids (CAA) namely tyrosine, phenylalanine, valine, leucine, isoleucine, were determined in 79 depressed females categorized according to the DSM-III. 2. In these patients the authors measured several parameters known to affect the availability of the above amino acids, i.e. triidothyronine (FT3) and thyroxine (FT4), vanilylmandelic acid (VMA), noradrenaline and adrenaline in 24 hr urine, the sex hormonal and nutritional state. 3. The 1 mg dexamethasone suppression test was performed and the pre and postdexamethasone cortisol and adrenocorticotropic hormone (ACTH) levels were determined at 8 a.m. 4. L-TRP and the ratio L-TRP/CAA were significantly lower in severely depressed females (296.X3, 296.X4) as compared with minor (300.40, 309.00) and simple major depressives (296.X2). The ratio L-TRP/CAA performed well as a clinical tool separating melancholic from minor depression. 5. FT3, FT4, VMA and noradrenaline were significantly increased in the severely depressed females, but these data did not correlate with the availability of L-TRP. Neither baseline cortisol nor the sex hormonal, nor the nutritional state related to the L-TRP data. The ratio L-TRP/CAA was significantly and negatively correlated with the postdexamethasone cortisol and ACTH values.
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PMID:The decreased availability of L-tryptophan in depressed females: clinical and biological correlates. 217 60

Plasma levels of the N-terminal peptide of proopiomelanocortin (NPP) were measured in rainbow trout, Salmo gairdneri, following treatment of handling stress with or without administration of dexamethasone, adaptation to white and black background, and maintenance on a constant light/dark cycle. Effects of exogenously administered NPP on plasma constituents were also examined to provide insight into the biological significance of NPP. Thirty minutes of handling stress in shallow water had no effect on plasma levels of NPP during and after the stress period, whereas significant increases in plasma cortisol and glucose were observed. Intraperitoneal administration of dexamethasone blocked the stress-induced elevation of plasma levels of cortisol and caused a depression of plasma NPP. No difference was observed in plasma levels of NPP between trout adapted to a white background and those adapted to a black background. No diurnal changes in NPP were observed under an artificial light/dark cycle (14L/10D light cycle, 0500-1900 hr light) in May and September. Thus, plasma levels of NPP were considerably constant under various physiological conditions, and no synchronism was observed between plasma NPP and cortisol, although NPP modifies the corticotropin-induced release of cortisol from the interrenal. Plasma constituents such as cortisol, total protein, albumin, plasma amino nitrogen, glucose, free fatty acid, ketone body, sodium, potassium, calcium, and magnesium were not altered by intraperitoneal injections of NPP (1 or 10 micrograms) once daily for 6 days (total of six injections) or once every other day for 28 days (14 injections). High concentrations of NPP were found in the plasma 24 hr after cessation of the serial injections of NPP (10 micrograms), suggesting slow metabolic clearance of the peptide.
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PMID:Plasma profiles of the N-terminal peptide of proopiomelanocortin in the rainbow trout with reference to stress. 229 28

The authors investigated the relationship between items on the Beck Depression Inventory and CSF levels of corticotropin-releasing hormone (CRH) in 17 depressed patients. Linear regression analysis showed that self-accusation, expectation of punishment, and crying accounted for 82% of CRH variance.
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PMID:Relationship of cognitive factors to CSF corticotropin-releasing hormone in depression. 230 55


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