Gene/Protein Disease Symptom Drug Enzyme Compound
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 130,125 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intravenously administered methylphenidate, 0.5 mg/kg, causes a consistent rise in human serum growth hormone level, with peak values usually occurring 30 minutes after infusion. This rise is attenuated in patients receiving various antipsychotic medications administered on a long-term basis and is decreased in schizophrenic and drug-dependent patients. Methylphenidate causes increases in talkativeness, blood pressure, and pulse that generally parallel increases in serum growth hormone level. However, in contrast to the methylphenidate-induced rise in serum growth hormone level, methylphenidate-induced changes in cardiovascular variables and talkativeness are not altered by antipsychotic medications or diagnostic classification.
Arch Gen Psychiatry 1978 Nov
PMID:The effect of methylphenidate on serum growth hormone: influence of antipsychotic drugs and diagnosis. 3 Apr 30

Abnormal anterior pituitary (AP) responsiveness to acute administration of thyrotropin-releasing hormone (TRH) and luteinizing hormone-follicle stimulating hormone-releasing hormone (LH-RH) was investigated in 14 patients (two men and 12 women) suffering from primary affective disorders. In ten, TRH, 500 microgram given intravenously, induced a rise in plasma growth hormone (GH) level, while in eight patients it induced a rise in plasma levels of FSH or LH or both. When LH-RH, 150 microgram was administered intravenously to ten patients, it induced a rise in plasma GH level in one patient and increased plasma prolactin level in three patients. Collectively, in only three of 14 patients was conventional AP responsiveness to hypothalamic neurohormones present. These findings demonstrate the existence of a profound derangement of AP responsiveness to hypothalamic neurohormones in depressed patients and suggest that a primary alteration in the physiologic links between the central nervous system and the AP may be at the origin of the neuroendocrine disturbance.
Arch Gen Psychiatry 1978 Oct
PMID:Deranged anterior pituitary responsiveness to hypothalamic hormones in depressed patients. 10 79

Chronic alcoholics with secondary depression were treated with protirelin in a double-blind, placebo-controlled study. Behavioral data, collected only during the acute alcohol withdrawal state, indicated a beneficial effect of protirelin three hours after injection, but not during subsequent days. Injections caused only mild and infrequent subjective side effects and no cardiovascular effects. Endocrine data were recorded in the acute withdrawal state and after clinical remission. Findings in the acute state suggested thyroid activation and increased central dopaminergic activity, as evidenced by elevated baseline levels of growth hormone, low baseline levels of prolactin, and blunted thyroid-stimulating hormone (TSH) response to protirelin. The first two abnormalities returned to normal levels in the remission state. A blunted TSH response was observed in both the acute and the remission states. Partial persistence of this finding suggests that TSH blunting may not be solely state-dependent. In the acute withdrawal state, TSH blunting was associated with favorable behavioral responses to protirelin.
Arch Gen Psychiatry 1979 May
PMID:TRH (protirelin) in depressed alcoholic men. Behavioral changes and endocrine responses. 10 8

We studied the effects of intravenous protirelin (thyrotropin-releasing hormone) in 17 schizophrenic patients and 17 normal subjects. A total of 12 patients received protirelin, 0.5 mg, and, on another occasion, niacin, 2 mg, in a double-blind, crossover design. Both behavioral and endocrine data were collected. Five patients received protirelin in an open trial; only endocrine data were collected. Protirelin caused about a 50% prompt decrease in psychotic symptoms. Patients then tended slowly to experience a relapse. Side effects were about as infrequent after protirelin as after niacin. We assayed serum prolactin (PRL), growth hormone (GH), thyroid-stimulating hormone (TSH), L-triiodothyronine (T3) and thyroxine (T4). Free T4 (FT4) index was calculated. The values for PRL, GH, and TSH at baseline and after protirelin stimulation were normal. Patients showed lower T3 values at baseline, but a brisker T3 response to protirelin, than controls. Their FT4 indices were higher at baseline. Patients showed diminished T4 binding sites rather than increased total T4. The causes of these alterations in thyroid dynamics are unidentified.
Arch Gen Psychiatry 1979 Sep
PMID:Behavioral and endocrine responses of schizophrenic patients to TRH (protirelin). 11 44

Investigation was undertaken on a patient whose long-term intake of desipramine hydrochloride was amongst the highest reported. Desipramine treatment instituted at a daily dosage of 75 mg for depressive equivalents of head, chest, and abdominal pain was increased to 1,000 mg daily over a 12-year interval with minimal side effects. Plasma desipramine level dropped immediately on withdrawal, and urinary metabolite values dropped over the subsequent five days. The electrocardiographic abnormalities of first-degree atrioventricular block and incomplete left bundle branch block rapidly disappeared on cessation of medication. Electroencephalographic changes with symmetrical generalized irregular 5- to 7-cps theta activity and 18- to 28-cps beta activity also improved. Longitudinal polygraphic sleep studies showed prolonged rapid eye movement rebound and increased delta sleep coincident with withdrawal. It took ten days after cessation of desipramine for urinary 3-methoxy-4-hydroxyphenylglycol concentration to increase substantially. Although catecholamines are involved in growth hormone (GH) and cortisol regulation, no abnormalities were found in GH or cortisol levels.
Arch Gen Psychiatry 1978 Oct
PMID:Withdrawal from long-term high-dose desipramine therapy. Clinical and biological changes. 21 86

The value of neuroendocrine techniques for providing information regarding the pathophysiology of psychotic disorders is largely dependent on clarification of the relationships among psychologic state, neural activity, and neuroendocrine regulation. This study presents a strategy for examining the interface between neurochemical activity, psychologic state, and neuroendocrine regulation. Psychologic state and serum growth hormone (GH) and cortisol were monitored following administration of methylphenidate hydrochloride, a drug that appears to preferentially affect central dopamine regulation. While individuals varied in both their endocrine and psychologic responses to methylphenidate, the general effects were GH elevation, euphoria, and activation with elation, the most pronounced psychologic effect. Subjects who showed GH elevation became elated while those who did not show a GH response did not become elated. Elation and GH release following administration of methylphenidate may be mediated by the same neurochemical events.
Arch Gen Psychiatry 1977 Sep
PMID:Psychologic and neuroendocrine response to methylphenidate. 90 Nov 39

A study of the tuberoinfundibular dopamine tract was undertaken in chronic schizophrenic patients with and without tardive dyskinesia. Biochemical evidence of the purported dopamine receptor supersensitivity in tardive dyskinesia was sought by demonstrating a hyperresponse of growth hormone and prolactin to dopamine agonists. Contrary to this prediction, no endocrine supersensitivity occurred in the tardive dyskinesia patients. Rather, a significantly decreased response to dopaminergic stimulation was demonstrated in the total chronic schizophrenic group.
Arch Gen Psychiatry 1977 Oct
PMID:A neuroendocrine study of supersensitivity in tardive dyskinesia. 91 Dec 19

Several pharmacological stimulation tests of the pituitary-hypothalamic system have been used to investigate psychiatric disorders. This study introduces amphetamine sulfate as a stimulus for human growth hormone (HGH) release in various psychiatric patients. Peak HGH release after a single intravenous administration of amphetamine sulfate, 0.1 mg/kg, was significantly lower in nine "endogenous" depressives (P = .01) and significantly higher in seven "reactive" depressives (P less than .05) as compared to normal subjects, whereas peak HGH release in eight schizophrenics and six chronic alcoholics did not differ significantly from that in normal subjects.
Arch Gen Psychiatry 1976 Dec
PMID:Reduced growth hormone responses to amphetamine in "endogenous" depressive patients: studies in normal, "reactive" and "endogenous" depressive, schizophrenic, and chronic alcoholic subjects. 99 50

Human growth hormone (HGH) responses to insulin-induced hypoglycemia were measured in ten postmenopausal women suffering from primary unipolar depressive illness, and in ten age-matched normal postmenopausal women. The mean maximal HGH response in the depressed patients was 4.6 plus or minus 4.4 ng/ml, and in the normals 13.3 plus or minus 9.8 ng/ml (P less than .05). All of the normal subjects had clinically adequate HGH responses, in contrast to only four of the depressed patients (P less than .01). The blood glucose responses were virtually the same in the two groups. Since brain catecholamines play a major role in mediating HGH responses to hypoglycemia, the findings are consistent with the hypothesis of diminished functional catecholaminergic activity in the depressed patients.
Arch Gen Psychiatry 1975 Jan
PMID:Growth hormone responses to hypoglycemia in postmenopausal depressed women. 111 75

After ingestion of 500 mg of levodopa, postmenopausal women had significantly diminished human growth hormone (HGH) responses (mean, 4.6 ng/ml), as compared with those of age-matched men (mean, 9.1 ng/ml; P smaller than .05). The differences between the groups were not related to plasma dopa concentrations. The HGH responses to levodopa of age-matched unipolar and bipolar depressed men, and of unipolar depressed postmenopausal women, did not differ significantly from their respective normal control groups. Depressive illness of these types does not appear to affect the HGH response to levodopa, once the effect of the menopause is taken into account.
Arch Gen Psychiatry 1975 Apr
PMID:Human growth hormone response to levodopa. Relation to menopause, depression, and plasma dopa concentration. 111 1


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