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)

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.
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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.
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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.
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PMID:Growth hormone neurosecretory disfunction in major depressive illness. 884 18

Changes in food intake, serum adipsin, and obesity were evaluated in the MSG-treated mouse. In Experiment 1, mice treated with MSG had 50% lower serum adipsin and over 2-fold higher percentage of body fat than the lean controls. Both feeding caffeine and restricting intake normalized serum adipsin and caused weight loss, but did not normalize the percentage of body fat. No additional effect was gained by feeding isoproterenol or ephedrine in combination with caffeine. In Experiment 2, we separated the direct effect of caffeine from the associated depression in intake using a paired feeding design, and also determined the effects of selected adrenergic agents and somatotropin (S). Somatotropin increased weight gain and reduced the percentage of body fat in healthy and obese mice, and tended to lower serum adipsin. Caffeine clearly depressed intake, caused weight loss, and increased serum adipsin, but similar results were achieved by restricting intake. None of the adrenergic drugs tested changed serum adipsin. Ephedrine depressed food intake and caused weight loss, but reduced the percentage of body fat only at the highest dietary concentration (2000 mg per kg of diet). Phenylephrine reduced weight gain without a concomitant effect on the percentage of body fat, and isoproterenol did not influence weight gain or body fat.
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PMID:Regulation of adipsin and body composition in the monosodium glutamate (MSG)-treated mouse. 891 74

Four experiments were conducted to elucidate the effects of porcine somatotropin (pST, growth hormone) on circulating testosterone concentrations in boars. In Exp. 1, jugular-cannulated obese boars were administered 4 mg recombinant (r) pST/d for 24 d before collection of samples at 15-min intervals over 6 h for measurement of pST, testosterone, and LH. Somatotropin treatment decreased plasma concentrations of testosterone and LH (P < .05). In Exp. 2, White composite boars were administered rpST with implants (4 mg/d) for 10 to 28, 16 to 28, or 22 to 28 wk of age. Reductions in testosterone concentrations were proportional to the length of time rpST was administered; boars treated for 18 wk had the lowest testosterone concentrations. Concentrations of LH declined throughout the study in rpST-implanted boars but remained static in untreated, control boars. In vitro production of testosterone and dehydroepiandrosterone/dehydroepiandrosterone sulfate was unaffected by rpST treatment, and hCG stimulation of in vitro androgen secretion was similar in rpST and control treatments. In Exp. 3, i.v. injection of pituitary pST (USDA-B1; 5 micrograms/kg BW) into jugular-cannulated White composite and Meishan boars resulted in an acute increase in circulating LH followed by an increase in testosterone concentrations, which then declined to below preinjection levels at 6 to 7 h after pST injection. Multiple injections, two or four per day, of 5 micrograms pST/kg BW resulted in decreased testosterone concentrations in White composite boars, whereas in Meishan boars testosterone concentrations were unaffected (Exp. 4). Concentrations of LH were not different from control values in either breed, but in both breeds, four injections of pST per day produced lower LH concentrations than did two injections per day (P < .01). Depression of circulating concentrations of androgens in boars requires extended periods of pST treatment.
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PMID:Effects of porcine somatotropin on circulating testosterone concentrations in boars and mechanism of action. 899 15

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.
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PMID:Specificity of the pyridostigmine/growth hormone challenge in the diagnosis of depression. 934 32

Administration of hormones to humans and animals results in specific effects on the sleep electroencephalogram (EEG) and nocturnal hormone secretion. Studies with pulsatile administration of various neuropeptides in young and old normal controls and in patients with depression suggest they play a key role in sleep-endocrine regulation. Growth hormone (GH)-releasing hormone (GHRH) stimulates GH and slow wave sleep (SWS) and inhibits cortisol, whereas corticotropin-releasing hormone (CRH) exerts opposite effects. Changes in the GHRH:CRH ratio contribute to sleep-endocrine aberrations during normal ageing and acute depression. In addition, galanin and neuropeptide Y promote sleep, whereas, in the elderly, somatostatin impairs sleep. The rapid eye movement (REM)-nonREM cycle is modulated by vasoactive intestinal polypeptide. Cortisol stimulates SWS and GH, probably by feedback inhibition of CRH. Neuroactive steroids exert specific effects on the sleep EEG, which can be explained by gamma-aminobutyric acid(A) receptor modulation.
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PMID:Effects of hormones on sleep. 955 Jan 12

1. Growth hormone (GH) secretion during sleep was studied in ten male patients with major depression according to DSM III and eight normal controls. 2. Samples were collected through a continuous blood withdrawal pump while sleep was recorded in the laboratory. 3. The results showed a marked decrease in the GH secretion mainly during the first three hours of sleep in depressed patients as compared to normal controls. DST and TRH tests were also administered to the same patients but no correlation was observed between a positive test and a blunted GH secretion, suggesting that the various neuroendocrinological disturbances do not coexist in all depressed patients. 4. This disturbance in GH secretion during sleep, along with reduced slow wave sleep (SWS), gives support to the theory that GHRH is the common stimulus of SWS and GH release and that the ratio of GHRH and its counterpart CRH plays a major role in the pathophysiology of disturbed endocrine activity during sleep in depression.
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PMID:Growth hormone secretion during sleep in male depressed patients. 961 44

We evaluated body weight loss and growth hormone secretion in patients with sleep-disordered breathing associated with chronic obstructive pulmonary disease. Of 11 patients hospitalized for pulmonary rehabilitation, five (WL group) had a history of body weight loss within two years before their interviews, while the other 6 patients (NWL group) had no changes in body weight. All patients underwent body index measurements, pulmonary function tests, blood gas analyses, assessments of nutritional status, and full night polysomnography for two consecutive days. Growth hormone levels were measured in the first 3-hour period following falling asleep. There were no significant inter-group differences between the results of pulmonary function tests, blood gas analyses, or nutritional status assessment. The WL group had a significantly higher percentage loss of body weight than the NWL group (mean +/- S.D. 11.5 +/- 4.7% in the WL group versus 2.7 +/- 1.8% in the NWL group, p < 0.01). The WL group had a significantly higher sleep apnea/hypopnea index than the NWL group (42.4 +/- 9.5/hr in the WL group versus 7.8 +/- 2.9/hr in the NWL group, p < 0.01). The WL group showed a higher rate of stage I + II sleep than the NWL group (84.9 +/- 7.0% versus 64.5 +/- 8.7%), with lower rates of slow wave sleep (2.2 +/- 2.1% versus 15.0 +/- 8.7%) and rapid eye movement sleep (12.9 +/- 6.3% versus 20.6 +/- 1.0%). The WL group showed a low level of growth hormone secretion with no peak in the sequential curve, but had a higher level of insulin growth factor-1 than the NWL group (148 +/- 36 ng/ml versus 90 +/- 22 ng/ml, p < 0.01). These results suggest that chronic obstructive pulmonary disease patients undergoing weight loss are likely to have an increase of growth hormone secretions in the daytime, possibly induced by underlying psychiatric disorders such as depression. Patients with chronic obstructive pulmonary disease may lose weight regardless of nutritional status because of a disturbance of growth hormone secretion resulting of sleep-disordered breathing.
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PMID:[Relationship between sleep disordered breathing and body weight loss in patients with chronic obstructive pulmonary disease]. 1279 81

Cortisone acetate, hydrocortisone, and hydrocortisone acetate depress the resistance of mice to pneumococcal and influenza viral infections, although hydrocortisone acetate is somewhat less effective than the free alcohol, when given subcutaneously. Pituitary adrenocorticotropin, even in highly purified form and in oil and beeswax, does not significantly alter the resistance of mice to these experimental infections, even when given in doses which may cause profound eosinopenia, lymphopenia, and weight loss, and which are at the limit of tolerance of the animals. Corticosterone depresses resistance to pneumococcal infections significantly, but fails to alter resistance to influenza viral infections. The findings suggest that murine adrenals may produce one of the known adrenal steroids such as corticosterone along with another steroid, or may produce a steroid other than cortisone, hydrocortisone, or corticosterone. When resistance is decreased by adrenal steroids, survival time is invariably shortened, and the effect of the steroid hormones is frequently demonstrable within the 1st day after infection with pneumococci, making it unlikely that the depression of resistance that is seen is primarily due to depression of antibody formation. A single dose of 5 mg. of cortisone may cause depression of resistance and may decrease the survival time for 3 to 6 days afterward. Growth hormone (somatotropic hormone) in highly purified form, and in the doses used, did not overcome the weight loss induced by cortisone, but the animals treated with growth hormone and cortisone regained their lost weight more rapidly than those receiving cortisone alone. Growth hormone alone caused a slight increase in the rate of gain in weight over controls. Growth hormone alone did not increase resistance to infection, and did not increase the survival time, in mice infected with either pneumococci or influenza virus. Growth hormone in various dosages failed to overcome the effect of cortisone in depressing resistance to these infections. Cortisone, hydrocortisone, corticosterone, and corticotropin did not alter significantly the titers of influenza virus attained in the murine lungs during the first 2 days after infection, but cortisone and hydrocortisone markedly delayed the rate at which virus titers declined during the subsequent 6 days. Corticosterone and corticotropin delayed the rate at which the titers declined but slightly, and growth hormone had no apparent effect, as compared with controls. Growth hormone did not overcome the effect of cortisone and hydrocortisone on viral titers. No detectable antibody was found as late as 6 days after infection, in controls or in hormone-treated animals.
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PMID:The effect of adrenal steroids, corticotropin, and growth hormone on resistance to experimental infections. 1311 66


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