Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A detailed review of the hormonal effects on intraocular pressure is presented. There is evidence that corticotropin, vasopressin, thyroxin, insulin, glucocorticoids and mineralocorticoids may play a role in the physiologic regulation of intraocular pressure. Growth hormone, melanocyte stimulating hormone, progesterone, estrogen, chorionic gonadotropin and relaxin may influence intraocular pressure when administered in pharmacologic doses. Whether the key to understanding primary open-angle glaucoma lies in recognizing abnormal endocrine mechanisms, especially involving glucocorticoids, remains unclear at the present time.
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PMID:Hormonal regulation of intraocular pressure. 41 3

To ascertain whether the dawn phenomenon occurs in normal adolescents and, if so, to determine its mechanism, we measured nocturnal plasma glucose, insulin, glucagon, growth hormone, cortisol, and adrenocorticotropic hormone (ACTH) levels between 01.00 and 08.00 h in 10 healthy adolescents. The prehepatic insulin secretion rate was calculated based on C peptide levels. The metabolic clearance rate of insulin (MCRI) was calculated as the ratio of mean insulin secretion rate to mean insulin concentration. There was no change in plasma glucose, insulin, and glucagon between 01.00-04.00 and 05.00-08.00 h (paired t test). The MCRI was higher at 05.00-08.00 h compared to 01.00-04.00 h (9.30 +/- 1.50 vs. 4.87 +/- 1.11 ml.kg-1.min-1; p = 0.008). The prehepatic insulin secretion increased at 05.00-08.00 h relative to 01.00-04.00 h (1.1 +/- 0.2 vs. 0.6 +/- 0.1 pmol.kg-1.min-1; p = 0.013). Similarly, cortisol and ACTH levels were higher at 05.00-08.00 versus 01.00-04.00 h (323 +/- 33 vs. 102 +/- 22 nmol/l, p less than 0.001; 3.6 +/- 0.5 vs. 1.8 +/- 0.4 pmol/l, p = 0.006, respectively). Growth hormone was higher at 01.00-04.00 versus 05.00-08.00 h (7.6 +/- 1.2 and 3.0 +/- 0.9 microgram/l; p = 0.019). ACTH correlated with MCRI (r = 0.66; p = 0.002) and prehepatic insulin secretion (r = 0.75; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Demonstration of a dawn phenomenon in normal adolescents. 196 21

Positive emotional activities have been suggested as modifiers of neuroendocrine hormones involved in the classical stress response. To detect changes in these components during a mirthful laughter experience, the authors studied 10 healthy male subjects. Five experimental subjects viewed a 60 minute humor video and five control subjects did not. Serial blood samples were measured for corticotropin (ACTH), cortisol, beta-endorphin, 3,4-dihydrophenylacetic acid (dopac)--the major serum neuronal catabolite of dopamine, epinephrine, norepinephrine, growth hormone, and prolactin. Repeated measures analysis of variance showed that cortisol and dopac in the experimental group decreased more rapidly from baseline than the control group (p = 0.011, p = 0.025, respectively). Epinephrine levels in the experimental group were significantly lower than the control at all time points (p = 0.017). Growth hormone levels in the experimental group significantly increased during baseline (p = 0.027) and then decreased with laughter intervention (p less than 0.0005), whereas, the controls did not change over time (p = 0.787). ACTH, beta-endorphin, prolactin, and norepinephrine levels did not significantly increase. The mirthful laughter experience appears to reduce serum levels of cortisol, dopac, epinephrine, and growth hormone. These biochemical changes have implications for the reversal of the neuroendocrine and classical stress hormone response.
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PMID:Neuroendocrine and stress hormone changes during mirthful laughter. 255 17

Two weeks following a single exposure to either soman (100 micrograms/kg, sc) or saline, rats were sacrificed at 2-hr intervals over a 26-hr period. Trunk blood was collected and plasma was stored until assayed for corticosterone, prolactin, growth hormone, adrenocorticotropin, beta-endorphin, and beta-lipotropin. Rats surviving for 2 weeks following soman appeared well groomed and were gaining weight at a rate similar to saline-treated rats at the time of termination. Thus, they appeared to have recovered from the initial physiological effects of soman exposure. However, substantial differences in plasma levels of most hormones were seen in comparing soman- vs saline-treated rats. Levels of prolactin were suppressed at all time points in soman-treated rats. Growth hormone secretion was also suppressed and the normal episodic peaks of growth hormone were missing in soman-treated rats. Both soman- and saline-treated rats displayed circadian rhythms in levels of plasma corticosterone, but the usual late afternoon rise in plasma corticosterone levels was shifted to earlier time points in the soman-treated rats. Levels of beta-endorphin and beta-LPH were slightly but significantly suppressed in soman-treated rats at almost all time points. Levels of adrenocorticotropin were similar in control and soman-treated rats. The results of this experiment demonstrate that a single exposure to soman may have long-lasting effects on neuroendocrine function.
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PMID:Long-term sequelae of soman exposure: hormonal rhythms two weeks postexposure to a single dose. 283 32

Concentrations of insulin, glucagon, growth hormone, adrenocorticotropin, and cortisol were determined in plasma samples obtained at 20-min intervals for 6 h from low and high producing dairy cows at d 30 and 90 postpartum. Four nonpregnant, nonlactating cows also were sampled. Insulin concentrations were reduced at d 30 in both groups of lactating cows compared with concentrations in nonlactating cows; glucagon concentrations were unchanged. The molar insulin: glucagon was reduced at d 30 in both groups and at d 90 for low, but not high producers. Growth hormone concentrations were higher at d 30 in high producers than at d 90, in low producers at d 30, and higher than in nonlactating cows. Cortisol concentrations were lower in high producing cows at d 30 than at d 90 or in nonlactating cows due to a reduced pulse amplitude. No differences were observed for adrenocorticotropin. Reduced molar insulin: glucagon may be an integral response of the cow to lactation, while the difference in the insulin: glucagon for high and low producers at d 90 postpartum may indicate a continued need for a gluconeogenic stimulus in low producers. The elevated growth hormone and low cortisol concentrations likely participate in the enhanced production observed in high producing dairy cows.
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PMID:Plasma concentrations of metabolic hormones in high and low producing dairy cows. 283 86

Many metabolic hormones (glucagon, hydrocortisone, corticosterone, TSH, thyroxine and triiodothyronine) did not stimulate porcine adipose tissue lipolysis in vitro. Growth hormone and ACTH stimulated lipolysis at high concentrations, in the presence of theophylline. Insulin inhibited lipolysis. Infusion of metabolic hormones with measurement of plasma free fatty acid and glycerol concentrations, purportedly indicative of in vivo lipolysis, indicated that glucagon and somatotropin had no effect, adrenocorticotropin increased and insulin depressed plasma concentrations of the metabolites. Overall, the in vitro predicts the in vivo response. There were exceptions, e.g. adrenocorticotropin moderately increased plasma metabolites but had little effect in vitro.
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PMID:Acute effects of metabolic hormones in swine. 287 Aug 58

We studied whether the previously reported intensified beta-endorphin response to exercise after training might result from a training-induced general increase in anterior pituitary secretory capacity. Identical hypoglycemia was induced by insulin infusion in 7 untrained (VO2max 49 +/- 4 ml X (kg X min)-1, mean and SE) and 8 physically trained (VO2max 65 +/- 4 ml X (kg X min)-1) subjects. In response to hypoglycemia, levels of beta-endorphin and prolactin immunoreactivity in serum increased similarly in trained (from 41 +/- 2 pg X ml-1 and 6 +/- 1 pg X ml-1 before hypoglycemia to 103 +/- 11 pg X ml-1 and 43 +/- 9 pg X ml-1 during recovery, P less than 0.05) and untrained (from 35 +/- 7 pg X ml-1 and 7 +/- 2 pg X ml-1 to 113 +/- 18 pg X ml-1 and 31 +/- 8 pg X ml-1, P less than 0.05) subjects. Growth hormone (GH) was higher 90 min after glucose nadir in trained (61 +/- 13 mU X l-1) than in untrained (25 +/- 6 mU X l-1) subjects (P less than 0.05). Levels of thyrotropin (TSH) changed in neither of the groups. It is concluded that, in contrast to what has been formerly proposed, training does not result in a general increase in secretory capacity of the anterior pituitary gland. TSH responds to hypoglycemia neither in trained nor in untrained subjects. Finally, differences in beta-endorphin responses to exercise between trained and untrained subjects cannot be ascribed to differences in responsiveness to hypoglycemia.
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PMID:The effect of training on responses of beta-endorphin and other pituitary hormones to insulin-induced hypoglycemia. 293 92

Recent studies showed that both the pineal gland and the endogenous opioid system are involved in the modulation of the immune system and in the regulation of tumor growth. Moreover, a relationship between pineal and opioid system has been demonstrated. In order get an overall view of the psychoneuroendocrine interactions in cancer patients, the levels of melatonin, the most important pineal hormone, and of beta-endorphin have been measured on blood samples collected during the morning. The study was carried out on 54 patients, 42 healthy subjects, and in 34 patients having illnesses other than cancer. Breast cancer, lung carcinoma, and colorectum cancer were the three neoplasms detected in the patients investigated. Growth hormone (GH), somatomedin-C and prolactin (PRL) levels were also determined. beta-endorphin levels were found to be substantially within the normal range in patients with cancer, whereas those of melatonin were raised in several cases. The beta-endorphin/melatonin ratio was higher than 2 in normal subjects, in non-neoplastic patients and in most cancer patients without metastases, whereas this ratio was lower than 2 in almost all patients in a metastatic stage of the disease. Neither melatonin levels nor those of beta-endorphin appeared to be significantly correlated with GH, somatomedin-C, and PRL concentrations. The low beta-endorphin/melatonin ratio observed in metastatic patients suggests the presence of an unbalanced relation between the pineal and the opioid system in those subjects. Therefore, an anomalous relationship between pineal function and opioid activity might play a role in the clinical course of neoplastic disease.
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PMID:A study on the relationship between the pineal gland and the opioid system in patients with cancer. Preliminary considerations. 296 35

Plasma prolactin response to thyrotropin-releasing-hormone (TRH) stimulation was diminished in 30 patients with prolactinomas and 9 patients with acromegaly who had normal serum prolactin levels. There was no overlap of prolactin responses when compared with 32 control patients. Responses of ten patients with adrenocorticotropin (ACTH)-secreting pituitary tumors were similar to those of controls. Plasma growth hormone concentrations after TRH stimulation changed significantly in 28% of normal control and 20%, 25% and 50% of patients with prolactin-, growth hormone- and ACTH-secreting pituitary tumors, respectively. Our data suggest that the blunted TRH-induced rise in plasma prolactin levels in patients with prolactinomas and those with acromegaly may be related to humoral factor(s) affecting TRH receptor or postreceptor function. Growth hormone responses to TRH are nonspecific and should not be considered a marker for active acromegaly.
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PMID:Diagnostic value of thyrotropin-releasing-hormone stimulation in patients with pituitary tumor. 311 72

The hypothalamic-pituitary function of 93 children, who had received central nervous system (CNS) prophylaxis as part of their therapy for acute lymphocytic leukemia (ALL), and who remained in continuous complete remission, was evaluated retrospectively. Treatment regimens included--Group I: 31 subjects, intrathecal methotrexate (IT MTX); Group II: 31 subjects, IT MTX plus 2400 rad cranial irradiation; and Group III: 31 subjects, IT MTX and intravenous intermediate-dose methotrexate. Serum thyroid-stimulating hormone (TSH) and T4 levels were normal. All participants had normal adrenocorticotropic hormone (ACTH) secretion as assessed by plasma cortisol responses to insulin hypoglycemia. Urinary follicle-stimulating hormone (FSH) and luteinizing hormone (LH) excretion of pubertal and postpubertal patients (N = 37) was appropriate, except for one subject from Group I who had an abnormally high output of gonadotropins, and one from Group II who had abnormally low levels. Growth hormone (GH) responses were subnormal after sequential arginine-insulin stimulation as follows--Group 1: 3 of 31 patients; Group II: 6 of 25 patients; and Group III: 2 of 29 patients. Nevertheless, all children had normal linear growth. It was concluded that the three forms of CNS prophylaxis evaluated had no long-term adverse effect on TSH and ACTH secretion. FSH-LH production appears to be normal, but final judgment must await follow-up studies because 60% of the patients were prepuberteral or still receiving chemotherapy. Eleven patients had subnormal GH responses after pharmacologic stimulation of the pituitary, but long-term linear growth was unaffected.
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PMID:Hypothalamic-pituitary function of children with acute lymphocytic leukemia after three forms of central nervous system prophylaxis. A retrospective study. 375 92


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