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

Growth hormone (GH) responses to the alpha 2-adrenoceptor agonist clonidine and to GH-releasing hormone (GHRH) were measured in 12 patients fulfilling DSM-III-R criteria for major depressive disorder and in 12 age- and sex-matched controls. GH responses to clonidine correlated significantly with the GH responses to GHRH in the depressed patients as well as in the controls. Neither the responses to clonidine nor the responses to GHRH were significantly lower in depressed patients than in controls. Similarly, somatomedin-C (Sm-C) plasma concentrations and baseline GH concentrations were not different between the two groups. The data do not suggest that blunted GH responses to clonidine and/or GHRH represent specific features of depression.
 ...
PMID:Growth hormone response to growth hormone-releasing hormone and clonidine in depression. 749 27

Growth hormone (GH) plasma concentrations reflect a balance between stimulation via GH-releasing hormone and inhibition by somatostatin. Cholinergic agonists enhance GH release by inhibiting somatostatin secretion and in health, stimulated GH release undergoes diurnal variation. We investigated the influence of cortisol on pyridostigmine-induced GH responses by testing six patients with DSM-III-R major depression at 09.00 and 14.00 h. There were no differences in GH responses to pyridostigmine between 09.00 and 14.00 h despite a preservation of the circadian variation of cortisol levels. If cortisol plays an important role in regulating cholinergic activity one would expect the diurnal variation of pyridostigmine-induced GH release to be preserved. As it is not, a reasonable assumption to make is that the muscarinic supersensitivity observed in depression may be independent of the prevailing steroid milieu.
 ...
PMID:Loss of the diurnal variation of pyridostigmine-induced growth hormone responses in depression: the effect of cortisol. 767 52

In view of the extensive use of anthelmintics in sheep and the fact that their activity may in part depend upon the immune system, we were interested to determine if ivermectin had any influence on aspects of the sheep immune response. Ten parasite-free 6-month-old lambs were drenched with ivermectin and 1 day later were given intravenously human erythrocytes and subcutaneously ovalbumin. Ten other lambs with injected antigens were not drenched and served as controls. Both groups were bled at intervals for cells and serum. The procedure was repeated on day 28. Lymphocytes from the drenched lambs, cultured in vitro in RPMI plus 50% autologous serum collected up to 7 and 14 days after the first and second antigen injections respectively, had decreased blastogenic activity compared with lymphocytes from control lambs. Similar results were obtained with lymphocytes cultured in RPMI 1640 supplemented with 50% autologous serum plus concanavalin A (Con A) or phytohaemagglutinin (PHA). When washed, lymphocytes were cultured in RPMI 1640 supplemented with 5% foetal calf serum (FCS) or 5% FCS plus Con A or PHA, decreased blastogenesis was observed but blastogenesis depression was not as marked as that observed with autologous serum. Similar antibody responses were seen for the drenched and control groups in response to the two injections of both antigens except that after the second injection, there was a significant reduction in antibody response to ovalbumin in the ivermectin-treated lambs. There were no differences in serum complement or serum nitric oxide levels between the two groups at any stage, but insulin-like growth factor-1 levels were significantly reduced in serum of the ivermectin-treated group, 4 days after each drench. Growth hormone levels were consistently significantly higher 22 days after both drenchings. There was no difference in mean body weight increase between the groups during the experiment.
 ...
PMID:Influence of ivermectin on cellular and humoral immune responses of lambs. 774 11

Young rats were fed on an essential fatty acid (EFA)-deprived diet for 6 weeks after weaning. Their pituitary was removed and adenohypophyseal cells dispersed and maintained in culture. Membrane lipids were analyzed and basal and stimulated levels of hormone secretion were measured after 4-day incubation in a culture medium containing or not 160 microM arachidonic acid 20:4n-6 (AA) in order to obtain EFA-deficient or EFA-restored pituitary cells, respectively. In EFA-deficient cells membrane phosphoglycerides (PGL) were depleted in AA and adrenic acid 22:4n-6; the deficit was overcome by incubation in the presence of AA. Depletion diversely affected PGL classes. AA was highly depleted in choline phosphoglycerides (ChoPG), only moderately depleted in serine and ethanolamine phosphoglycerides (SerPG and EtnPG) and not depleted at all in inositol phosphoglycerides, suggesting preferential preservation of AA in that class of PGL. Restoration of AA by addition of the fatty acid to the culture medium was complete for ChoPG and EtnPG and only partial for SerPG. Depressed levels of AA and adrenic acid in PGL were compensated for by a concomitant increase in 20:3n-9 and 22:3n-9. Growth hormone and prolactin (PRL) secretion was assessed by radioimmunoassay and possible effects of a membrane AA deficit on hormone regulation were tested in cells challenged by either growth hormone-releasing hormone, thyrotropin-releasing hormone, angiotensin II (AII), vasoactive intestinal peptide (VIP) or dopamine. Neither basal nor stimulated growth hormone secretion was different from controls in EFA-deficient cells. PRL modulation by VIP or dopamine was not affected either in EFA-deficient cells. In contrast, the capacity of AII, but not of thyrotropin-releasing hormone, to release PRL was markedly decreased in EFA-deprived cells. It was restored by addition of AA to the incubation medium. Parallel depression of AII-induced inositol phosphates and cAMP accumulation was also observed after EFA deficiency. When tested on membranes, the paradoxical inhibition of adenylate cyclase by AII documented by previous observations was reinforced in EFA-deficient membranes. In contrast, binding of AII was not affected by EFA deficiency. It is concluded that under our experimental conditions EFA deficiency affects selectively coupling of the AII receptor to its effectors without alteration of binding. The effect could involve changes in receptor interactions with coupling proteins.
 ...
PMID:Selective effect of a diet-induced decrease in the arachidonic acid membrane-phospholipid content on in vitro phospholipase C and adenylate cyclase-mediated pituitary response to angiotensin II. 782 82

We report a 64-year-old patient suffering from rapid cycling bipolar disorder who was studied by means of polysomnography, neuroendocrine tests and PET (positron emission tomography) imaging. In a manner only partly compatible with the cholinergic-aminergic imbalance model of mania and depression, a linkage of REM sleep disinhibition and depressive mood was observed, but no decisive REM sleep delay was seen on manic days. Growth hormone secretion after clonidine stimulation was blunted on depressive and hypomanic days. A series of total sleep deprivations led to a positive effect on psychopathology for about two weeks. Carbamazepine treatment normalized REM sleep variables, damped the amplitude of mood cycling of the patient, increased TSH and decreased FT4.
 ...
PMID:48-hour rapid cycling: results of psychopathometric, polysomnographic, PET imaging and neuro-endocrine longitudinal investigations in a single case. 835 69

Growth hormone (GH) secretion in the 100 minutes preceding sleep onset (preSO), as well as in the first half of the night (1st HN), was examined for a group of 13 healthy women and 43 women with recurrent depression who participated in a 3-year maintenance therapy study. GH studies were obtained at several points during treatment and every 3 months during maintenance, during which patients were randomly assigned to active drug or drug-free maintenance treatment cells for 3 years, or until recurrence of depression. Depressed patients were divided into subgroups according to their maintenance treatment assignment (active drug or drug free) and treatment outcome (completing in remission or having a recurrence). Imipramine caused an increase in the GH ratio in all subgroups. Protocol completers had a significantly larger imipramine-induced increase in the GH ratio than did recurrers. The difference in time of GH secretion relative to sleep onset was found to correlate with treatment outcome and was independent of medication status during maintenance.
 ...
PMID:Growth hormone secretion timing in depression: clinical outcome comparisons. 858 Feb 24

Growth hormone (GH) responses to growth hormone releasing hormone (GHRH) of 53 in-patients meeting DSM-III-R criteria for major depressive episode with melancholia (24 non-delusional and 23 delusional depression) were compared with those of 19 healthy controls. No significant differences in basal GH were found between the control and either the non-delusional or the delusional groups. The whole group of depressed patients showed a significantly lower response than the control patients at all points of the GH response to GHRH curve as well as a lower area under curve. When the three groups (control, delusional, and non-delusional depressed) were compared, it was found that only the non-delusional depressed patients had a significantly lower area under curve and lower values at +60, +90 and +120 min than the controls. The only significant difference between the two groups of depressed patients was that the delusional group showed a delayed appearance of the maximum response peak and a more prolonged response.
 ...
PMID:Growth hormone response to growth hormone releasing hormone in non-delusional and delusional depression and healthy controls. 868 86

In order to establish whether reported psychological complaints in hypopituitary adults are related to growth hormone (GH) deficiency or other pituitary hormone deficiencies, emotional well-being and cognitive performance were evaluated in 31 men with multiple pituitary hormone deficiencies (MPHD) and in 17 men with isolated growth hormone deficiency (IGHD). Assessments included evaluation of somatic and psychological complaints, depression, fatigue, vigor, tension, state and trait anxiety, iconic memory, short-term memory, long-term memory and perceptual-motor skill. The control group consisted of 41 healthy men, matched for age. Growth hormone secretion was more severely impaired in MPHD than in IGHD patients. Despite oral replacement therapy, MPHD patients also had lower serum testosterone levels than IGHD subjects. The MPHD patients were found to have lower vigor scores, higher state anxiety scores, worse perceptual-motor skill and worse memory performance than controls. In contrast, IGHD patients only showed subnormal memory performance. It was concluded, therefore, that the cognitive impairment in both MPHD and IGHD was related to GH deficiency. The subnormal vigor scores in MPHD patients were attributed to the reduced testosterone levels. The worse perceptual-motor skill in MPHD patients might be related specifically to ACTH deficiency. Finally, the higher state anxiety in MPHD was attributed to a low self-esteem, which may be the psychological consequence of the hypogonadal appearance these patients have. We conclude that, from a psychological point of view, MPHD and IGHD adult patients are quite distinct groups.
 ...
PMID:Cognitive impairments and mood disturbances in growth hormone deficient men. 881 29

Neurotransmitter impairments in MDI can also affect hormonal neuroregulation. Therefore, we decided to study the integrated concentration of growth hormone (IC-GH) and its 24-h secretory profile in this pathology. Ten women with major depressive illness (MDI) (three premenopausal and seven postmenopausal) and four normal matched controls (one premenopausal and three postmenopausal) were evaluated. Samples were obtained every 30 min using a constant withdrawal pump. Growth hormone (GH) pulses were analysed by Cluster System. Twenty-four hour IC-GH was evaluated as area under the curve (AUC) and the following results were found: depressed (D) = 429.15 +/- 367.9 vs. controls (C) = 1281.07 +/- 379.77 (p < .008); nocturnal IC-GH: D = 220 +/- 274.0 vs. C = 739.52 +/- 378.15 (p < .02). No statistically significant differences were found between D and C in diurnal IC-GH or in the number of nocturnal or diurnal pulses. Adrenal (cortisol at 0800h, 2300h and post-suppression with 1 mg of dexamethasone) and thyroid (T3, T4, 0800h and 1700h TSH) evaluations did not show statistically significant differences between D and C women. In conclusion, patients with MDI present a decrease in total GH secretion at the expense of the nocturnal period, probably due to changes in the neurotransmitters that would be involved in depression.
 ...
PMID:Growth hormone neurosecretory disfunction in major depressive illness. 884 18

Acetylcholine is a neurotransmitter that has been implicated in the pathophysiology of major depression. This is supported by the enhanced growth hormone (GH) release in response to pyridostigmine (PYD) challenge in depressed subjects relative to healthy comparison subjects. The aim of this study is to examine the specificity of the PYD/GH challenge in the diagnosis of depression. Pyridostigmine 120 mg orally, was administered to a total of 116 physically healthy subjects. Growth hormone responses were studied in 38 patients with (DSM-III-R) major depression, 13 subjects with panic disorder, 9 subjects with schizophrenia, 10 recently detoxified alcoholics, and a comparison group of 46 healthy volunteers. Mean delta GH (the difference between basal and maximal GH following PYD) was significantly greater than comparison subjects in patients with major depression. Responses observed in patients with schizophrenia and alcohol dependence syndrome did not differ from the comparison group. Those patients with panic disorder and a high Hamilton depression score had an enhanced delta GH. The sensitivity of the PYD/GH test was 63% for major depression. These results indicate that the PYD/GH test may help distinguish depression from schizophrenia, alcohol-dependence syndrome, or panic disorder with a low Hamilton depression score.
 ...
PMID:Specificity of the pyridostigmine/growth hormone challenge in the diagnosis of depression. 934 32


<< Previous 1 2 3 Next >>