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)

A variety of endocrine dysfunctions have been reported for anorexia nervosa, protein caloric malnutrition, and depression. The effect of reduced caloric intake and weight loss on endocrine functions was assessed in an experiment with five healthy female subjects during an initial baseline phase, a 3-week phase of complete food abstinence, weight gain to the original level, and a final baseline phase. During fasting, disturbances in hypothalamic-pituitary-adrenal function were observed, with elevated plasma cortisol levels, increase in the number of secretory episodes, increase in cortisol plasma half-life, and insufficient suppression following 1.5 mg dexamethasone. While all dexamethasone suppression tests (DSTs) were normal at baseline, 7 of 14 DSTs showed insufficient suppression in the fasting phase. During fasting, basal thyroid-stimulating hormone (TSH) values were lowered and the TSH response to thyrotropin-releasing hormone (TRH) was blunted. The plasma level of growth hormone (GH) over 24 hours was elevated during fasting and administration of the alpha 2-adrenergic receptor agonist clonidine resulted in a subnormal GH response after restoration of original body weight. One of the five subjects showed increased irritability, distress, anxiety, and depression as measured by various psychological scales. The results show that reduced caloric intake, weight loss, or catabolic state have powerful effects on several endocrine systems. The specificity of measures of endocrine disturbances (DST, TRH tests, and clonidine tests) as biological markers for certain types of depression must be questioned, and the metabolic state should be given more consideration in future studies.
 ...
PMID:Weight loss causes neuroendocrine disturbances: experimental study in healthy starving subjects. 308 Jul 66

The thyrotrophin-releasing hormone (TRH) stimulation test is becoming useful in the diagnosis of depression, but the optimum concentration of TRH required remains uncertain. The test was performed on a carefully selected group of patients with primary unipolar major depressive episodes with melancholia, who were severely depressed, using TRH 200 micrograms and 500 micrograms (groups 1 and 2). The thyroid-stimulating hormone (TSH), growth hormone (GH) and prolactin (PRL) levels were measured in response to TRH. Responses obtained were compared with respect to hormonal and genetic subgroups. Comparing groups 1 and 2 revealed significant differences in the GH responses (P = 0,0059). A similar significant difference was found in the GH response (P = 0,0102) elicited by the women in each group. Comparison of the genetic subgroups of groups 1 and 2 revealed a significant difference in the PRL response of both the genetic spectrum (P = 0,0258) and the group without a genetic history (P = 0,0259) of alcoholism or depression. The TSH response in the genetic spectrum group was also significantly higher (P = 0,0008) in group 2. Further investigations of the responses elicited in the different genetic subgroups may reveal important variables for the investigation of the pathogenesis of depression.
 ...
PMID:Genetic differences in the endocrine responses to the thyrotrophin-releasing hormone stimulation test in patients with a major depressive episode. 308 19

Several investigators have reported a paradoxical growth hormone (GH) response to thyrotropin-releasing hormone (TRH) in depressed patients, but other studies have failed to confirm this. In the present study, the GH response to TRH was studied in depressed patients and normal subjects. The rate of paradoxical GH response to TRH in depression was no different than that observed in control subjects. This was the case whether the data was examined using mean values or using frequency of abnormal responses. Patients with blunted thyrotropin (TSH) responses did not differ in GH release from patients with normal TSH response. A variety of factors may have contributed to the earlier reports of a positive GH response to TRH, including the definition of paradoxical GH release and the fact that depressed patients exhibit more frequent spontaneous diurnal GH release than do normal subjects.
 ...
PMID:Is there paradoxical growth hormone response to thyrotropin-releasing hormone in depression? 308 39

TRH-induced thyrotropin (TSH), prolactin (PRL), and growth hormone (GH) responses were investigated together with a dexamethasone suppression test in female psychiatric inpatients with major melancholic depression (n = 21), schizophrenic disorder (n = 20), alcohol dependence (n = 11), and adjustment disorder with predominantly depressed mood (n = 13), as well as in 15 healthy women. Abnormal responses for all four endocrine variables were noted most frequently in melancholia; however, a significant number of the non-depressed patients also had abnormal hormonal responses in the individual test. The association of two or three abnormalities proved to be quite specific for the melancholic group. There were no statistically significant differences in TRH-induced TSH responses among the patient subgroups. Non-suppression of cortisol after dexamethasone was associated with blunted TSH-responses only in melancholia. There was a tendency for non-suppressor schizophrenics to show more abnormal GH-responses to TRH administration.
 ...
PMID:Associations among dexamethasone non-suppression and TRH-induced hormonal responses: increased specificity for melancholia? 309 67

TRH tests were performed on 131 patients with RDC diagnoses of major depressive disorders to study altered endocrine control mechanisms in subtypes of depression. The TSH response to TRH was measured in all patients. In more than a third of the sample the prolactin (PRL) and growth hormone (GH) responses were also analysed. There were no differences between bipolar, primary unipolar and secondary unipolar patients in means of any endocrine variable. However, the expected positive correlation between baseline TSH and delta TSH was absent in the secondary unipolar group, indicating a dysregulation of pituitary TRH receptor sensitivity in this depressive subtype. Only delta TSH was dependent on depressive state, being lower in currently ill primary unipolar patients only. Patients with melancholic features (endogeneity scores high) had blunted TSH responses. Weight loss was connected with TSH blunting in all depressive subtypes. Among patients with blunted delta TSH (less than 5 mU/l) there was no relationship between degree of weight loss and delta TSH. Further, examination of partial correlation coefficients suggests weight loss of affect delta TSH by virtue of its being part of the melancholic syndrome. A significant correlation between blunted delta TSH and nonsuppression of cortisol in the DST was found only among primary unipolar patients, arguing for some independence of the TRH test and the DST in mirroring disturbed endocrine controls in depression.
 ...
PMID:TRH tests with analyses of TSH, prolactin, and GH responses in subtypes of patients with major depressive disorders. 309 81

In an evaluation of the possible role of dopamine on TRH test results, 21 depressed patients were given TRH before and after one week of treatment with a low dose of haloperidol. Haloperidol significantly increased serum prolactin (both basal and after TRH) and cortisol levels, decreased body temperature, and had no effect on serum TSH, growth hormone, or thyroid hormone levels. Five of six patients with initial TSH blunting were retested with TRH; in four patients the TSH response remained blunted. These data render it unlikely that dopamine exerts a major inhibitory input on TSH secretion in depression.
 ...
PMID:The TRH test during dopamine receptor blockade in depressed patients. 309 92

To explore the growth hormone-releasing hormone (GHRH)-GH-somatomedin axis in major depressive disorder, 12 patients and 12 normal controls matched to the patients on age, sex, ovarian status and body weight received synthetic human GHRH-44 amide (1 microgram/kg) as an intravenous bolus. Compared to controls, the depressed patients showed a reduction in baseline plasma GH and a significant attenuation of net plasma GH responses to GHRH. The blunted GH responses occurred along with significantly increased somatomedin C (Sm-C) concentrations. The impairment of GH responses to GHRH and the increased Sm-C concentrations in patients with depression could have resulted from episodic hypersecretion of GH during the daytime, indicating integrity of the negative feedback circuitry. Normal feedback regulation suggests that diurnal episodic hypersecretion of GH reflects an abnormality at or above the level of the hypothalamus, so that the GHRH-GH-somatomedin axis hyperactivity observed in certain patients with major depressive disorder may be due, at least in part, to hypersecretion of hypothalamic GHRH. Our failure to demonstrate a difference in plasma prolactin (PRL) responses to GHRH between controls and depressed patients indicates that GHRH is not a PRL releaser in patients with major depression and that the altered GH secretory dynamics may not be directly related to the altered circadian PRL secretion linked to depression.
 ...
PMID:Growth hormone (GH) and prolactin responses after GH-releasing hormone in major depressive disorder: relationship to somatomedin C levels and dexamethasone suppressibility of cortisol. 313 88

Twenty subjects (10 patients with major depressive disorder and 10 controls matched for age, gender, and ovarian status) received 1 microgram/kg synthetic human growth hormone-releasing hormone (GHRH)-44 amide as an i.v. bolus dose. Compared to controls, depressed patients showed a significant attenuation of net growth hormone (GH) responses to GHRH associated with normal basal GH concentrations. The blunted GH responses occurred in the face of significantly higher somatomedin C (Sm-C) concentrations. Comparison of GH responses after GHRH with GH output following the alpha 2-agonist clonidine (CLON) revealed a significant positive correlation. The concordance between GH responses after specific challenges at different levels of the GHRH-GH-somatomedin axis indicates the integrity of the hypothalamic-pituitary-somatotropic system in depression and supports the view that altered GH secretory patterns in depression may primarily be due to a suprapituitary disturbance.
 ...
PMID:Growth hormone (GH) responses to GH-releasing hormone in depression: correlation with GH release following clonidine. 314 43

The hepatic monooxygenase system was studied in hypophysectomized female rats infused for 5 days with ovine growth hormone (GH). At 7.5 micrograms.h-1 GH decreased the total cytochrome P-450 by 16%; at 10 micrograms.h-1 it reduced both cytochrome P-450 (31%) and the activity of ethylmorphine demethylase (31%). GH did not alter the activities of NADPH cytochrome c reductase or aniline hydroxylase. The lower GH dose decreased the amount of fast- and slow-turnover P-450 by 11 and 38%, respectively, while the higher dose decreased both by 49%. The loss of demethylase activity therefore correlates with the loss of fast-turnover P-450. This component is relatively more abundant in the female (fast: slow turnover of 4.3) than the male (fast:slow turnover of 2.5). GH did not affect the half-lives of the P-450 components, suggesting that it decreases their synthesis. The P-450 concentration in microsomes from GH-treated animals did not increase after incubation with hemin, suggesting that in vivo the hormone does not lower P-450 synthesis via depression of heme. Puromycin mimicked the effect of GH and when given with the hormone their effects on the P-450 levels were multiplicative (p less than 0.05), suggesting different modes of action and that GH does not decrease P-450 by acting at translation.
 ...
PMID:Growth hormone depresses ethylmorphine demethylase activity: correlation with decreased levels of fast-turnover cytochrome P-450 in hypophysectomized female rats. 314 99

We report on a new X-linked recessive syndrome in 2 unrelated families, consisting of pre- and postnatal growth excess, typical facial phenotype allowing diagnosis at birth, and usually normal physical and intellectual development. The minor anomalies seen at birth include a "coarse" face with wide nasal bridge, short nose with upturned nasal tip, wide open mouth, thick lips, midline depression of the lower lip, enlarged tongue, highly arched palate, large maxilla and jaw, and a short broad neck. Voice is hoarse and affected individuals have a plump, stocky body with pectus excavatum, thoracic scoliosis, hepatosplenomegaly, umbilical and/or inguinal hernias, broad short hands and feet, and in some cases preauricular dimples, abnormal ears, postaxial hexadactyly, hypoplastic index finger nails, and abnormal dermatoglyphics. Early postnatal death is frequent and pathogenetically unexplained. During infancy and childhood the leading manifestations are the overgrowth (greater than 97th centile), striking facial appearance, hypodontia and/or malposition of teeth, genua valga, hypoplastic calf muscles, and clumsiness. Adolescent and adult patients have well proportioned "gigantism" of athletic build (192-210 cm), large "coarse" face, and a deep voice. General intellectual and motor development are either normal or mildly delayed. Results of routine laboratory tests are normal, as are growth hormone and IGF I levels and chromosomes. Pathogenesis remains unknown. Heterozygotes may show some of the characteristic facial changes.
 ...
PMID:A new X-linked dysplasia gigantism syndrome: follow up in the first family and report on a second Austrian family. 317 54


<< Previous 1 2 3 4 5 6 7 8 9 10