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)

Patients with severe depression have been observed previously to have a reduced rate of glucose utilization accompanied by elevated serum insulin levels during the intravenous glucose tolerance test (GTT) and a reduced metabolic responsiveness to exogenous insulin during the insulin tolerance test (ITT). These abnormalities were less obvious in patients with neurotic depression as compared to patients with severe endogenous or "psychotic" depression. To evaluate more fully the relationships of depressive symptomatology to these metabolic abnormalities, patients were rated by nursing staff on a short clinical rating scale (SCRS) and by a psychiatrist on the Brief Psychiatric Rating Scale (BPRS) at the time the metabolic measurements were made. Patients were given the GTT and the ITT once when they were off medication and symptomatic and then again 3 to 8 weeks later when symptoms had decreased following amitriptyline treatment. Fasting serum-free fatty acid levels (FFA) had a significant positive correlation to rating of anxiety. Fasting levels of glucose, insulin, and human growth hormone (HGH) did not significantly correlate to any of the ratings. A decreased rate of glucose utilization (k) correlated significantly with increased ratings of motor retardation, emotional withdrawal, and blunt affects, but not to other depressive symptoms. The responsiveness of FFA and HGH during the ITT was significantly less in patients with more severe symptomatology; responsiveness improved when those patients improved. Neither incorrelated to the ratings. These data suggest that within the sydrome of depression, increased FFA is realated to anxiety, decreased glucose utilization is related to motor retardation, emotional withdrawal, and blunt affect, and that decreased FFA and HGH responsiveness to insulin is a nonspecific correlate of the general depressive syndrome.
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PMID:Depressive symptoms and the glucose tolerance test and insulin tolerance test. 119 11

Theorists have extrapolated the cholinergic supersensitivity theory of affective disorder from a convincing and broad spectrum of clinical observation and research. This hypothesis is tested using a neuroendocrine probe approach with the challenge drug pyridostigmine, an indirect cholinergic agent thought to release growth hormone (GH) by decreasing inhibitory somatostatin tone. The consequent increments in plasma GH were considered to reflect central acetylcholine responsivity. Fifty-four volunteers were tested: 27 DSM-III-R major depressives (18 women and 9 men) and 27 age- and sex-matched healthy controls. Subjects were cannulated at 9.00 h following an overnight fast and two baseline samples were taken at 15 min intervals. Pyridostigmine 120 mg was administered orally and thereafter samples were taken at the time points +60, +90, +120 and +180 min. GH responses were significantly greater in depressives than controls and this effect was more marked for men than women. These results support the proposal that muscarinic upregulation and/or supersensitivity is associated with depression.
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PMID:Pyridostigmine-induced growth hormone responses in healthy and depressed subjects: evidence for cholinergic supersensitivity in depression. 131 44

The effect of the alpha 2-adrenoceptor agonist, clonidine, on plasma growth hormone (GH), plasma 3-methoxy-4-hydroxyphenylethylenegylcol (MHPG), blood pressure and sedation were studied in 16 menopausal subjects before and 6 wk after a 100-mg implant of estradiol. The specific binding of tritiated yohimbine to intact platelets also was studied. Estradiol implants increased basal GH output and reduced baseline MHPG and sedation scores. However, none of the subsequent responses to clonidine were altered. Platelet yohimbine binding also was unchanged following the implant. Both observer- and self-rating scales showed a marked reduction in anxiety and depression scores. The results suggest that estradiol may alter some indices of noradrenergic function, but that the mechanism does not involve alterations in alpha 2-adrenoceptor sensitivity.
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PMID:Effect of estradiol implant on noradrenergic function and mood in menopausal subjects. 131 72

The aims of this study were to determine whether the administration of cortisol has a significant effect on mood in patients with depression and whether the effects of cortisol on changes in plasma hormone concentrations are like those of synthetic corticosteroids. Twelve patients had major depression and one each had dysthymic disorder and a depressive adjustment disorder. Five were male and nine were female. All were in-patients. Eight normal subjects, two females and six males, were used as controls. Basal beta-endorphin concentrations were 2- to 3-fold higher in depressed patients than in control subjects, but there were no significant differences between the patient and control groups in the basal (pre-infusion) plasma concentrations of ACTH, cortisol, growth hormone or prolactin. Cortisol, but not saline infusion resulted in a significant improvement in self rated mood. Surprisingly, cortisol infusion at first increased plasma beta-endorphin concentrations. At later times after cortisol infusion, plasma beta-endorphin concentrations decreased as did the plasma concentrations of ACTH and growth hormone; prolactin levels were increased. These results show (i) that cortisol infusion raises mood significantly in major depression, (ii) that plasma beta-endorphin concentration is a potential marker of major depression (iii) that rather than blunting of corticosteroid effects, responses to cortisol may even be enhanced in depressive illness. The unexpected, initial increase in beta-endorphin stimulated by cortisol, suggests that the action of cortisol is not simply one of negative feedback inhibition, but may involve mineralocorticoid, as well as glucocorticoid receptors.
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PMID:The effects of cortisol infusion upon hormone secretion from the anterior pituitary and subjective mood in depressive illness and in controls. 133 93

Immunological, neuroendocrine and psychological parameters were examined in 14 psychophysically healthy subjects and in 17 panic disorder patients before and after a 30-day course of alprazolam therapy. T lymphocyte proliferation in response to the mitogen phytohemagglutinin, lymphocyte beta-endorphin (beta-EP) concentrations, plasma ACTH, cortisol and beta-EP levels were examined in basal conditions and after corticotropin-releasing hormone (CRH) stimulation. Cortisol inhibition by dexamethasone (DST) and basal growth hormone (GH) and prolactin levels were also examined. Depression, state or trait anxiety, anticipatory anxiety, agoraphobia, simple and social phobias, severity and frequency of panic attacks were monitored by rating scales. The immune study did not reveal any significant difference between patients and controls, or any effect of alprazolam therapy. The hormonal data for the two groups were similar, except for higher than normal basal ACTH and GH plasma levels, lower than normal ratios between the ACTH and cortisol responses to CRH, and blunted DST in some patients. All the impairments improved after alprazolam therapy, in parallel with decreases in anxiety and in severity and frequency of panic attacks.
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PMID:Psychoimmunoendocrine aspects of panic disorder. 133 59

In 57 patients with psicovegetative disorders and abnormal MMPI, abnormality in MMPI scales indicating hypochondriasis, hysteria, gender deviant, paranoia, psychastenia, schizophrenia, hypomania or introversion was accompanied by increased plasma catecholamine levels and/or responses to hypoglycemia or by an increased cardiovascular reactivity. A high depression scale was associated with lower plasma catecholamine levels. Blunted plasma growth hormone responses to hypoglycemia were found in abnormal hypomania scale, and augmented responses of plasma cortisol in abnormal hysteria or schizophrenia scales. Paranoia and hypomania traits correlated with absence of morning-evening differences in blood cortisol levels. Electrodermal responses compatible with increased sympathetic activity correlated with high hysteria, gender, paranoia, schizophrenia or hypomania MMPI scales. This study indicates that most psychopathological traits in MMPI are accompanied by humoral and/or electrophysiological signs of abnormality of the autonomic nervous system.
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PMID:Some neurovegetative correlates of Minnesota Multiphasic Personality Inventory (MMPI) 136 36

Chronically fasted rainbow trout (Oncorhynchus mykiss) had significantly lower plasma L-thyroxine (T4) and triiodo-L-thyronine (T3), and higher plasma growth hormone (GH) concentrations than fed animals. Fasted and fed trout were administered bovine thyrotropic hormone (bTSH), native ovine GH (oGH), or recombinant human GH (rhGH) alone, or GH in combination with bTSH to further study the effects of food deprivation on the activity of the pituitary-thyroid axis and on the control of hepatic T3 production. Although the fasted rainbow trout retained the ability to respond to bTSH challenge, the resultant elevation in plasma T4 concentration was significantly lower than that of fed animals; there was no plasma T3 response to bTSH challenge in either fed or fasted trout, except for a significant elevation in fed bTSH-injected fish and a significant depression in fed saline-injected fish sampled 2.5 hr after the injection. GH when administered alone had no significant effect on plasma T4 concentrations of either fed or fasted animals, and stimulated an increase in plasma T3 concentration and an increased hepatic T3 content only in the fed fish, despite a significant stimulation by both oGH and rhGH of in vitro hepatic 5'-monodeiodinase activity (MDA) in both fed and fasted groups. bTSH appeared to suppress rhGH- and oGH-stimulated MDA in fasted groups, and rhGH-stimulated MDA in fed trout. The data suggest that chronic fasting induced a down-regulation of the response of thyroid tissue to bTSH challenge, and of the GH-stimulation of T3 production, in vivo, although in vitro hepatic MDA was elevated following GH administration to both fed and fasted rainbow trout.
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PMID:Chronic fasting reduces the response of the thyroid to growth hormone and TSH, and alters the growth hormone-related changes in hepatic 5'-monodeiodinase activity in rainbow trout, Oncorhynchus mykiss. 142 38

Physical training at high altitude improves performance at high altitude. However, studies assessing performance improvements at sea level after training at higher altitudes have produced ambiguous and inconclusive results. Hypoxia-induced secondary polycythemia is a major contributor to increased work capacity at altitude. The common finding upon exposure to hypoxia is a transient increase in haemoglobin concentration and haematocrit because of a rapid decrease in plasma volume followed by an increase in erythropoiesis per se. Both nonathletes and elite endurance athletes have maximal reticulocytosis after about 8 to 10 days at moderate altitude. Training periods of 3 weeks at moderate altitudes result in individual increase of haemoglobin concentration of about 1 to 4%. A more accentuated increase in haemoglobin can be obtained with longer sojourns at moderate altitude. The normal erythropoietin reaction upon exposure to hypoxia comprises initially increased levels followed by a decrease after about 1 week. Thus, the maintenance of a high erythropoietin concentration is not a prerequisite for a sustained increase in erythrocyte formation at high altitude. The main pharmacological modulator of erythropoietin production seems to be adenosine. But modulators such as growth hormone and catecholamines may also potentiate the effect of hypoxia per se on erythropoietin production. On the other hand, there is a risk that the stress hormones may induce a relative depression of the bone marrow particularly in the early phase of altitude training when the adaptation is minimal and the stress reaction is most accentuated. The most important 'erythropoiesis-specific' nutrition factor is iron availability which can modulate erythropoiesis over a wide range in humans. Adequate iron stores are a necessity for haematological adaptation to hypoxia. However, at moderate altitude, there is a need for rapid mobilisation of iron and even if the stores are normal there is a risk that they cannot be mobilised fast enough for an optimal synthesis of haemoglobin. Data from healthy athletes training at moderate altitudes suggest a true increase in haemoglobin concentration of about 1% per week. Complete haematological adaptation occurred when sea level residents have similar haemoglobin concentrations at moderate altitude compared with residents. The normal difference in haemoglobin concentrations can be estimated to be about 12% between permanent residents at sea level and at 2500m above sea level. This difference indicates a necessary adaptation time of about 12 weeks. If the training period at moderate altitude must be shorter, several sojourns at short intervals are recommended. The important factor in haematological adaptation in athletes at moderate altitude is hypoxia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:High-altitude training. Aspects of haematological adaptation. 143 97

The neuroendocrine response to L-5-hydroxytryptophan was compared in 37 prepubertal children who met the Research Diagnostic Criteria for major depressive disorder with that in 23 normal children with no lifetime history of any psychiatric disorder and very low rates of depression in both first- and second-degree relatives. Intravenous L-5-hydroxytryptophan (0.8 mg/kg) was given over a 1-hour interval after preloading with oral carbidopa, an inhibitor of peripheral but not central L-5-hydroxytryptophan metabolism. L-5-Hydroxytryptophan, a precursor of serotonin, increases serotonin turnover in the central nervous system when given after carbidopa. Seven (19%) of the 37 children with major depressive disorder and two (9%) of the 23 normal children had nausea or vomiting and therefore did not complete the full infusion. They were subsequently excluded from data analysis. After this stimulation, prolactin, cortisol, and growth hormone secretion were compared between diagnostic groups. The depressed children secreted significantly less cortisol (effect size, 0.70) and significantly more prolactin (effect size, 0.83). There was a sex-by-diagnosis interaction in prolactin response to L-5-hydroxytryptophan and, on examination, the prolactin hypersecretion was seen in depressed girls but not in depressed boys compared with same-sex controls. There was no significant stimulation of growth hormone in either group. These findings are consistent with dysregulation of central serotonergic systems in childhood major depression.
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PMID:Neuroendocrine response to L-5-hydroxytryptophan challenge in prepubertal major depression. Depressed vs normal children. 144 21

Several lines of evidence suggest that dopamine might be involved in anxiety states. In this study, we assessed the growth hormone (GH) response to apomorphine (a dopaminergic agonist) 0.5 mg SC in nine drug-free inpatients meeting Research Diagnostic Criteria (RDC) for panic disorder who were age-matched and gender-matched with nine major depressive, and nine minor depressive inpatients. The three groups differed significantly in their mean GH peak response: 5.29 +/- 2.75 ng/ml in major depressives, 26.27 +/- 12.71 ng/ml in minor depressives, and 37.28 +/- 10.58 ng/ml in panics, with a significantly higher response in panic than in either minor or major depressive patients. These results support dopaminergic overactivity in panic disorder as compared with major and minor depression.
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PMID:Dopaminergic function in panic disorder: comparison with major and minor depression. 146 80


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