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)

Somatostatin is a tetradecapeptide that is assuming increasing importance as a regulator of central nervous system activity. Originally identified as the hypothalamic growth hormone release-inhibiting factor, somatostatin has subsequently been shown to be extensively and selectively distributed throughout the central nervous system, to alter neuron excitability, to regulate and be regulated by the activity of classical neurotransmitters and neuropeptides, to exert a number of direct behavioral actions, and to display neuropsychiatric disorder-related alterations. In this article, a three-part study of cerebral spinal fluid (CSF) somatostatin in affective illness and schizophrenia is presented. In part 1, significant reductions in CSF somatostatin were observed in 49 bipolar and unipolar depressed patients relative to 47 controls. Values during depression were also significantly lower than those observed in affective disorder during the improved state or in schizophrenia. Diurnal studies involving paired AM and PM lumbar punctures revealed that depressed patients and normal volunteers had similar somatostatin values in the evening, despite having significantly different values in the morning. In part 2, the effects of several psychopharmacological agents on CSF somatostatin were examined, particularly the tricyclic anticonvulsant carbamazepine. A significant reduction of CSF somatostatin during treatment with carbamazepine was observed. The effect of carbamazepine on somatostatin could be related to its anticonvulsant, analgesic, or psychotropic effects. Part 3 deals with somatostatin as a major regulator of hypothalamic-pituitary-adrenal (HPA) axis activity. Somatostatin affects HPA activity by inhibiting, at a number of cellular levels, the stimulated release of adrenocorticotrophic hormone (ACTH) from the pituitary. A significant negative relationship between CSF somatostatin and the postdexamethasone plasma cortisol level in 22 depressed and 16 schizophrenic patients was observed. This relationship between low CSF somatostatin and escape from dexamethasone suppression was observed irrespective of diagnosis (i.e., depression or schizophrenia). Thus, there is indirect supporting evidence for a role for somatostatin dysregulation in the most consistently observed biological abnormality in depression, escape from dexamethasone suppression. Further study of somatostatin in neuropsychiatric disorders, and particularly depressive illness, offers great promise for better understanding their underlying affective, vegetative, cognitive, and physiological dysregulations.
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PMID:Cerebrospinal fluid somatostatin and psychiatric illness. 286 90

Plasma concentrations of oestrogen-stimulated neurophysin (ESN), prolactin, and growth hormone were measured before and after the first treatment in a course of electroconvulsive therapy (ECT) given to 25 psychiatric patients and during induction of anaesthesia in 9 women undergoing elective cholecystectomy. Prolactin levels rose and growth hormone levels fell during both cholecystectomy and ECT, but ESN levels rose only after ECT. The peak ESN response to ECT was significantly greater (p less than 0.005) in the 16 depressed patients who recovered than in the 9 who did not. All patients in whom plasma ESN concentration increased by more than 100% satisfactorily recovered from their depressive illness. If a 63% increase in ESN concentration is used to classify all subjects, 12% are misclassified by outcome at 2 months. The extent of the ESN response, but not the prolactin or growth hormone responses, correlated with improvement in symptoms measured by Hamilton Rating Scale for Depression and the Montgomery and Asberg Depression Rating Scale.
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PMID:Oestrogen-stimulated neurophysin and outcome after electroconvulsive therapy. 287 18

Piribedil, a dopaminergic agonist, was administered intravenously (0.5 mg over 10 minutes) to two unipolar endogenous depressed. The two patients, a 38-year-old man and a 60-year-old woman, were matched for age and sex with two volunteers without any mental illness. Effects of piribedil on plasma levels of growth hormone and on blood pressure were studied. The two volunteers evaluated their "feelings" of anxiety and of physical comfort using visual analogue scales. The experimentation was repeated in a double blind fashion with a placebo. Piribedil induced an elevation of GH in the normal man but not in the depressed man. In contrast, no increase was noted in women. No elevation of GH was observed after placebo. Importance of factors such as depression, sexual steroid environment and influence of stress are discussed.
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PMID:[Stimulation of somatotropin hormone by piribedil, a dopaminergic agonist, in endogenous depression. Preliminary study]. 290 10

The effects of single and repeated electroconvulsive treatment (ECT) on beta-endorphin (beta-EP), cortisol, growth hormone (GH) and prolactin (Prl) plasma levels were investigated in nine depressed patients. Blood samples were monitored a day before ECT, the day of the first and sixth ECT (0, 30, 60 and 90 min after seizures), the day afterwards and 4 weeks after termination of the ECT course. A significant elevation of beta-EP levels was achieved immediately with and 24 h after the first and the sixth ECT. A transient increase in basal beta-EP was observed 1 day following the sixth ECT in comparison with pre-treatment level. Peak and 30 min levels of cortisol were increased compared with baseline by the first ECT. The former (peak) but not the latter (30 min) were increased also at the sixth treatment. GH levels were decreased the day after the first ECT in comparison with the pre-treatment levels and immediately following each ECT in comparison with baseline. A trend toward elevation of Prl was observed immediately after the first and sixth ECT, although the rise did not reach significant levels. ECT administration stimulated beta-EP and cortisol secretion and suppressed human GH release, possibly by activation of endorphinergic and/or serotonergic systems. These mechanisms might be involved in the beneficial effect of ECT in depression.
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PMID:The effect of acute and repeated electroconvulsive treatment on plasma beta-endorphin, growth hormone, prolactin and cortisol secretion in depressed patients. 295 20

Desipramine 75 mg i.m. was given in the morning to 20 adolescents with major depressive disorder and 23 normal controls. Depressed adolescents secreted significantly less growth hormone (GH) over the next 2 h than did normal adolescents, although a substantial proportion of the differences were accounted for by the depressed adolescents who had a specific suicidal plan or attempt during the episode. Severity of depression or the presence of other depressive symptoms did not predict GH secretion within the depressed group. Age, sex and maturational factors in the control of GH are discussed. It is concluded that these differences in GH secretion probably reflect differences in CNS beta-adrenergic and/or serotonergic function. Suicidality and depression may have different psychobiological correlates in adolescents.
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PMID:Growth hormone response to desmethylimipramine in depressed and suicidal adolescents. 297 4

Basal serum cortisol, growth hormone, prolactin and immunoreactive (IR) plasma beta-endorphin levels were measured in 31 depressed patients (14 endogenous, 17 nonendogenous) undergoing the dexamethasone suppression test. The endogenously depressed patients had significantly higher (22.55 +/- 1.34 micrograms/dl) predexamethasone cortisol levels than the nonendogenous patients (16.34 +/- 1.93 micrograms/dl). The mean serum prolactin and growth hormone values of these two groups were not significantly different, while plasma IR-beta-endorphin levels of the endogenous group (40.11 +/- 3.57 pg/ml) were significantly lower than those of the nonendogenous group (120.33 +/- 27.98 pg/ml). Neither group showed a significant correlation between plasma IR-beta-endorphin and serum cortisol values. These results indicate that measurement of predexamethasone serum cortisol values and plasma IR-beta-endorphin could be valuable laboratory tests in the diagnosis of depression.
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PMID:Plasma levels of beta-endorphin, cortisol, prolactin and growth hormone in depressed patients. 297 11

Although clinically undistinguishable, some authors have found important differences in the counterregulatory response between Biosynthetic Human Insulin (BHI) and Purified Pork Insulin (PPI). To reassess the problem 10 healthy volunteers of both sexes underwent paired iv insulin tolerance test with both BHI and PPI (0.10 U/kg b.w.). To check the humoral response the variations of glucose, free fatty acids (FFA), prolactin, growth hormone, ACTH and plasma renin activity were evaluated. Blood glucose depression and further recovery by BHI and PPI administration paralleled each other, so were, prolactin, FFA, and plasma renin activity. A slight section of ACTH, and GH was observed under BHI challenge. There were not statistically significant differences between both insulins on any of the six parameters studied. The data do not confirm earlier published reports indicating hormonal and metabolic differences between human and porcine insulin.
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PMID:Metabolic and hormonal parameters after insulin-induced hypoglycemia in man, comparison between biosynthetic human insulin and purified pork insulin. 299 43

Superior cervical ganglionectomy (SCG X) decreased significantly serum growth hormone (GH) levels in rats 14-96 h after surgery, during and immediately after anterograde degeneration of regional sympathetic terminals. At later times (up to 28 days after SCG X) an increase in serum GH was observed. SCG X augments prolactin (PRL) release, but only at the earliest time examined (14 h after surgery). Injection of the alpha-adrenoceptor blocker, phenoxybenzamine, but not of the beta-blocker, propranolol, negated the depression in serum GH found in SCG X rats 14 h after surgery, without affecting PRL release.
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PMID:Changes in growth hormone and prolactin release after superior cervical ganglionectomy of rats. 300 57

The authors review the literature in an attempt to evaluate the relationship between serotonin and depression. Animal studies show that the administration of tryptophan (the precursor of serotonin) increased serotonin synthesis and influenced behavior. Low plasma tryptophan levels have been found in patients with endogeneous depression. Postmortem studies have shown an association between lowered hindbrain serotonin levels and suicide among depressed persons. The decreased serotonin levels in blood platelets during depression mirrored the neuronal changes. Tricyclic antidepressants inhibited platelet serotonin uptake and reduced imipramine binding sites on the platelets. A positive correlation between depression rating scores and platelet aggregatory response has been reported. Serotonin stimulated release of prolactin and growth hormone, although the prolactin response was less marked in depression. A marker for depressive illness is still sought, but it is likely to be related in some way to serotonin.
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PMID:Serotonin and its place in the pathogenesis of depression. 304 11

1. The present paper reports the effects of dietary modifications on the diurnal pattern of concentrations of certain metabolites and hormones in the peripheral blood of lactating dairy cows. The cows were given fixed rations of hay and high-cereal concentrates in the proportions of 30:70 or 10:90 (w/w). The concentrates were given in either two or six equal meals daily; the hay was given twice daily. 2. Previous reports of the same experiment had shown that milk-fat yield and concentration were reduced by increasing the proportion of concentrates in the diet and increased by more frequent feeding of the concentrates. These changes could be explained in part by changes in rumen volatile fatty acid (VFA) proportions and mean daily concentrations of VFA, particularly propionic acid, and insulin in the peripheral blood, but these factors failed to explain all the increase in milk-fat concentration caused by more frequent feeding. 3. Analysis of blood samples taken at hourly intervals for 24 h at two stages of lactation showed that, in the cows fed six times daily, the concentrations of metabolites and hormones remained relatively constant over the day. In the cows fed twice daily, the concentrations of VFA, 3-hydroxybutyric acid and insulin all increased after both meals whereas the concentrations of glucose and growth hormone tended to fall. The concentration of non-esterified fatty acids tended to increase overnight and fall rapidly after the morning feed. The concentrations of glucagon, thyroxine and prolactin showed no clear pattern in relation to meals. The postprandial responses of propionate, insulin and growth hormone were greater with the higher concentrate diet. 4. The maximum concentration and the diurnal range of concentrations were reduced by more frequent feeding of both diets in the case of propionic acid and of the higher concentrate diet in the case of insulin, but the effects on insulin concentrations of more frequent feeding of the lower concentrate diet were smaller and not significant. The maximum concentration and the diurnal range of concentrations of growth hormone were unaffected by meal frequency. 5. It is concluded that the severity of milk-fat depression in cows fed twice daily is increased by the rapid rise in propionic acid concentration in the peripheral blood after a meal, which in turn increases insulin secretion and may be accompanied by a suppression of growth hormone release. This causes lipogenesis to be diverted towards adipose tissue at the expense of the mammary gland.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Feeding frequency for lactating cows: diurnal patterns of hormones and metabolites in peripheral blood in relation to milk-fat concentration. 305 1


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