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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of intravenous somatostatin on blood levels of metabolites and hormones has been examined in normal subjects who performed a 30-minute period of bicycle exercises at 70% maximal exercise capacity. The results have been compared with control studies in the same subjects. Measurements were made of blood levels of lactate, glucose, free fatty acids, glycerol, acetoacetate, 3-hydroxybutyrate, insulin, glucagon, growth hormone (hGH) and prolactin. Growth hormone and glucagon release were suppressed during exercise with somatostatin and there was a subsequent elevation during recovery. There was slight post-exercise depression of insulin, but no alteration of plasma prolactin secretion. Blood glucose was reduced during exercise with somatostatin and increased during recovery. The elevation of ketone bodies after exercise was greater in the investigation with somatostatin, but there were no significant changes in other metabolites. Somatostatin, although causing inhibition of hGH release, appeared to have no significant effect upon fatty acid mobilization during exercise.
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PMID:The effect of somatostatin on metabolic and hormonal changes during and after exercise. 47 77

Twenty-five depressed patients were examined as to their growth hormone responses to TRH. An enhanced pituitary growth hormone response to intravenous injection of 500 mug TRH was observed in eight depressed patients, while TRH administration did not raise growth hormone levels in nine of 10 normal subjects examined. Occurrence of enhanced response of growth hormone was not related to the thyrotropin values after TRH administration. Bipolar patients exhibited enhanced growth-hormone response more frequently than unipolar patients. Five patients with involutional depression and neurotic depression who showed the most insufficient thyrotropin release to TRH administration together with lowered thyroid function revealed to be non-responders of growth hormone.
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PMID:Enhanced growth hormone responses to TRH injection in bipolar depressed patients. 81 72

Interest in possible neuroendocrine disturbances in endogenous depression is prompted by two lines of evidence: (1) clinical features of the illness suggest hypothalamic dysfunction; (2) the brain neurotransmitters implicated in depression also regulate neuroendocrine function. Our research reveals a marked, sustained hypersecretion in cortisol in severe depressive illness, which is apparently unrelated to stress and sleep disturbance, and which is associated with a distortion of the 24-hour cortisol secretory pattern. The hypersecretion is manifested primarily in the late afternoon, evening, and early morning hours, when cortisol secretion is normally inhibited. Growth hormone responses to hypoglycemia (but not to L-dopa) are also significantly reduced in endogenous depression, even when factors of age and the menopause are controlled. Postmenopausal depressed women appear to secret significantly less LH than normal postmenopausal women. Since all of these hormonal abnormalities can be reproduced by depletion of brain noradrenalin, the findings provide support for the the hypothesis of reduced functional noradrenergic activity in certain forms of depression.
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PMID:Neuroendocrine studies of depressive illness. 98 19

This study was designed to clarify the details of any changes in serum growth hormone levels occurring in surgical patients. Intravenous glucose tolerance tests were performed upon three groups of six patients each, Group I, minor surgery (inguinal herniorrhaphy), Group II, moderate surgery (vagotomy and pyloroplasty), and Group III, major surgery (aortofemoral bypass). Plasma glucose and serum growth hormone levels were measured. Depression of glucose utilization occurred together with elevations of fasting growth hormone levels and increased growth hormone responses to intravenous glucose. It is suggested that the increased serum growth hormone levels are a response to the glucose intolerance caused by operation, modifying the pituitary growth hormone release.
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PMID:The effect of surgical operation on growth hormone levels in plasma. 114 26

Twelve depressed adolescents and 12 controls matched for age, sex, Tanner stage, time of menstrual cycle (females), weight, and time of year assessed were studied over 3 nights. Measurements for cortisol, thyroid stimulating hormone, and growth hormone were made on serum collected at 10 P.M., 12 midnight, 1 A.M., 2 A.M., 3 A.M., 4 A.M., and 6 A.M. in eight pairs and every 20 minutes from 8 P.M. to 7 A.M. in four pairs. Cortisol secretion did not significantly differentiate the groups. Thyroid stimulating hormone secretion was significantly elevated in the depressed group at one time point. Growth hormone secretion significantly differentiated the two groups at most time points, and the depressed adolescents significantly hypersecreted growth hormone (area under the curve). Implications for the diagnosis, etiology, and treatment of adolescent depression are discussed.
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PMID:Nocturnal cortisol, thyroid stimulating hormone, and growth hormone secretory profiles in depressed adolescents. 178 55

Growth hormone (GH) response to clonidine and growth hormone-releasing hormone (GHRH) stimulation, together with baseline somatomedin C (SmC) levels, were examined in parallel in a group of 21 patients with anorexia nervosa (AN) and in 10 controls. In addition, the Hamilton Rating Scale for Depression (HRS) was administered to the patients. Clonidine (2.5 micrograms/kg body weight, iv) induced GH elevations that were not significantly different between patients and controls. In contrast, GHRH (1 microgram/kg body weight, iv) produced a significantly higher GH response in anorectics than in controls. The ratio between GH responses (area under the curve, or AUC) to GHRH and to clonidine was significantly higher in patients than in controls. Baseline SmC levels (6 patients) were significantly lower in anorectics than in controls. Minor depressive symptomatology was present in all patients. When viewed in relation to the GH hyperresponsiveness to GHRH, the apparent normality of the response to clonidine in anorectics reflects the existence of an actual alpha 2-adrenoceptor subsensitivity. As clonidine reportedly acts via release of endogenous GHRH, an excessive, rather than a normal, GH response to clonidine was to be anticipated.
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PMID:Alpha 2-adrenoceptor sensitivity in anorexia nervosa: GH response to clonidine or GHRH stimulation. 253 61

Growth hormone (GH) responses to the alpha 2-adrenoceptor agonist guanfacine and to GH releasing hormone (GHRH) were measured in 13 patients fulfilling Research Diagnostic Criteria and DSM-III criteria for major depressive disorder and in 13 controls matched for age and sex. Dexamethasone suppression tests were performed in all subjects. The peak GH response to guanfacine correlated to the peak GH response to GHRH both in depressed patients and in controls. Neither the response to guanfacine nor the response to GHRH was significantly lower in depressed patients than in controls. Dexamethasone suppression tests, which were performed about 3 days before the GH stimulation tests, were abnormal in 61% (8/13) of the depressed patients but in none of the controls. No difference between dexamethasone suppressors and nonsuppressors with respect to GH response to guanfacine or GHRH was observed. The data are discussed in relation to the blunted GH response to clonidine described in depression.
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PMID:Growth hormone responses to the alpha 2-adrenoceptor agonist guanfacine and to growth hormone releasing hormone in depressed patients and controls. 290 63

The effect of adenohypophysial hormones on rat pineal melatonin content and release was examined in vitro. Medium concentration of radioimmunoassayable melatonin decreased after a 6 h exposure to 1-100 ng/ml FSH; pineal levels of melatonin were only decreased by 100 ng/ml FSH. LH (1-100 ng/ml) augmented significantly medium melatonin concentration, tissue levels being increased at 10 ng/ml LH. Parallel increases of explant and medium melatonin content were found after exposure to 1-100 ng/ml TSH. At the smallest concentration employed (1 ng/ml) prolactin increased melatonin content and release while at 100 ng/ml a significant depression of both parameters was found. Growth hormone (1-10 ng/ml) augmented melatonin levels in medium but failed to modify them at 100 ng/ml, although at this concentration tissue melatonin levels increased. ACTH did not modify pineal melatonin synthesis in vitro.
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PMID:In vitro effects of adenohypophysial hormones on rat pineal melatonin content and release. 303 98

Preliminary results are presented from a series of studies designed to characterize the regulation of release/metabolism and receptor responsiveness in the noradrenergic and serotonergic systems in acutely depressed patients and depressed patients in remission. Abnormal regulation of noradrenaline release/metabolism might be expected to be associated with the acute state of depression, while abnormalities of adrenoceptor responsiveness were hypothesized to persist in remission. Growth hormone responses to clonidine were measured as indices partially reflecting alpha 2-adrenoceptor responsiveness. Blunted responses to clonidine were found in both acutely depressed patients and patients in remission. The possible implications of these findings for the pathophysiology of the noradrenergic system in depression are discussed. Prolactin responses to the serotonergic agonist and serotonin-releasing agent fenfluramine were evaluated in acutely depressed patients, patients in remission and controls. A subset of the depressed patients appeared to have blunted prolactin responses to fenfluramine. However, very preliminary results do not show any difference in this response between patients who were acutely ill and those in remission, although the variability in both groups was great. These and related findings are discussed in terms of a possible contributory role of the serotonergic system in depression.
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PMID:Adrenergic and serotonergic receptor responsiveness in depression. 381 11

The effects of iontophoretically applied human pancreatic growth hormone-releasing factor (hpGRF), peptide histidine isoleucine (PHI-27), and somatostatin (SS) on the extracellular activity of single cells in the hypothalamus, thalamus, and cortex of the rat brain were studied in urethane-anesthetized, male rats. Neurons with membrane sensitivity to hpGRF, PHI-27, and SS were present in each brain region. Although neurons excited by these peptides were encountered in thalamus and hypothalamus, depression of neuronal firing was the predominant response observed. Overall, the neurons responding to hpGRF also possessed membrane sensitivity to PHI-27, whereas, the hpGRF sensitive neurons appeared to be more divided as to their ability to respond to SS. The results clearly demonstrate that hpGRF and PHI-27 are capable of affecting the membrane excitability of neurons in several brain regions. The distribution of neurons sensitive to hpGRF suggests that hypothalamic GRF, in addition to its well documented role in the regulation of pituitary growth hormone secretion, may subserve other physiological events in the rat central nervous system as a neurotransmitter and/or neuromodulator.
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PMID:Sensitivity of rat forebrain neurons to growth hormone-releasing hormone. 393 50


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