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)

In sheep and other ruminants parturition is stimulated by increased secretion of fetal cortisol. The mechanism of this increased fetal adrenal activity is not known, but may be dependent on a decreased fetal hypothalamopituitary sensitivity to the negative feedback inhibition by cortisol. Seven fetal sheep (129-142 days gestation), chronically prepared with vascular catheters, were infused with cortisol (10 micrograms/min; n = 5) or vehicle (n = 4) for 5 h. Cortisol infusion increased fetal plasma cortisol to 50.8 +/- 4.3 ng/ml, approximately 33 ng/ml above the corresponding plasma cortisol concentration in the vehicle-infused fetuses. One hour after the end of the cortisol or vehicle infusion, infusion of sodium nitroprusside (50 micrograms/min, iv) increased fetal plasma adrenocorticotropin hormone (ACTH) concentration in both groups of fetuses. Results of another study (15) demonstrated that increases in fetal plasma cortisol of only 1.7 ng/ml for 5 h in younger (117-131 days gestation) fetuses completely blocked the fetal ACTH response to the same dose of nitroprusside. The results indicate that the preparturient rise in fetal ACTH is accompanied by a decrease in cortisol negative feedback.
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PMID:Does a decrease in cortisol negative feedback efficacy precede ovine parturition? 382 22

SJL/J mice which developed a high incidence of spontaneous reticulum cell neoplasms, developed a low rate incidence (20-25%) of myeloid leukemia (ML) after X-irradiation. The possible effect of adrenal steroid imbalance to radiation-induced ML in SJL/J mice was tested. Intact and thymectomized animals were exposed to a single dose of 300 r whole body irradiation and treated with either hydrocortisone acetate, prednisone, metyrapone and adrenocorticotropin as coleukemogenic agents. Hydrocortisone and prednisone exerted a marked coleukemogenic effect, increasing the ML incidence to a similar rate of about 50-70%, at a mean latent period of 300 days. Prominent leukemic infiltration were observed in the bone marrow, spleen, lymph nodes and liver of the leukemic animals. Results of cytological and histological studies, including cytochemistry and ultrastructure, were all consistent with the diagnosis of acute myeloid leukemia (AML). Since AML is the type of human secondary leukemia which appears increasingly in patients treated with alkylating drugs and/or irradiation and corticosteroids for Hodgkin's disease or other neoplastic diseases, the experimental model of AML induced in SJL/J mice could be used for elucidation of mechanisms of leukemogenesis in secondary leukemia.
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PMID:High incidence of acute myeloid leukemia in SJL/J mice after X-irradiation and corticosteroids. 386 24

Plasma membrane sacs of isolated rat fat cells (ghots) possess an adenyl cyclase system, which is activated by lipolytic hormones of disparate molecular structure, including adrenocorticotropin (ACTH), glucagon, and epinephrine. Previous studies indicated that distinctive selectivity units for individual hormones are coupled to the same unit of adenyl cyclase in the fat cell membrane. The present study has shown that ghost cyclase from adrenalectomized and hypophysectomized rats exhibits a striking reduction in response to ACTH, the stimulatory effects of epinephrine, glucagon, or fluoride being unchanged. Pretreatment of adrenalectomized, hypophysectomized, sham operated, or intact rats with the synthetic glucocorticoid, dexamethasone, selectively increased the ACTH response in ghost cyclase preparations. Cortisol, like dexamethasone, increased the ACTH response in ghosts from adrenalectomized rats; 11-deoxycorticosterone was ineffective. The dexamethasone effect to enhance the ACTH response is blocked by actinomycin D or cycloheximide. The present results show that stimulation of rat fat cell adenyl cyclase by ACTH involves a distinctive molecular entity, which can be clearly differentiated from adenyl cyclase in the membrane as well as from the selectivity sites for epinephrine and glucagon. The data indicate that the biosynthesis of the component required for ACTH stimulation of ghost cyclase-either an ACTH selectivity unit or specific coupling factor-is induced by glucocorticoids at the level of gene regulation.
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PMID:Glucocorticoid regulation of ACTH sensitivity of adenyl cyclase in rat fat cell membranes. 431 84

The heptadecapeptide ACTH 1-17 is the analogue of corticotropin with beta-alanine in position 1, lysine instead of 17-arginine and a basic amide instead of 18 arginine-amide. These modifications give enhanced biological activity and longer duration of the action. Several researchers investigated the acute effect of the analogue after administration at different time points along the 24 h cycle, and discovered that glucocorticoid and mineralocorticoid responses are dissociated in terms of doses and timing. Cortisol and urinary 17 OH-CS rise more after morning injections whereas for aldosterone the maximum effect was noted at 14(00). The most interesting finding that concerns ACTH 1-17 is the chronizing effect. ACTH 1-17 can be a chronizer because its administration resets, for instance, the toleration to antimitotic drugs, to a more convenient time. At clinical level, a group of researchers studied, in some case correctly from a chronobiological point of view, the effect of the ACTH 1-17 on patients and on healthy subjects. It is useful to remember the concept of hierarchies of rhythms: each different periodic function is regulated or, better, intermodulated by a network of other periodic variables of the same organ or of other organs and systems. So the necessity of large samplings to evidentiate periodic phenomena, and the utility of investigating pertinent marker rhythms significantly correlated with those to be studied are evident. Autorhythmometry and automatic monitoring can help very much on this purpose.
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PMID:Heptadecapeptide ACTH 1-17: the first analogue in chronobiology. 609 Dec 36

Blood was drawn from 14 normal volunteers twice before, immediately after a 1-minute immersion of the nondominant hand in ice water (cold pressor test), and twice during recovery. Serum levels of beta-endorphin, cortisol, prolactin, growth hormone, and opioid activity were determined, and measures of subjective pain appraisal and coping styles were obtained. Cortisol was the only variable to show a significant increase as a function of noxious stimulation. Correlational analysis yielded relationships between neuroendocrine variables and subjective pain appraisal as well as coping styles, suggesting complex interactions between neuroendocrine and psychological processes in human pain.
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PMID:Endocrine effects of the cold pressor test: relationships to subjective pain appraisal and coping. 609 73

Corticotropin and hydrocortisone were studied for their effect on dehydrogenase activity of microbial E. coli cells in the medium with the tricarboxylic acid cycle substrates, glucose and beta-oxybutyric acid. Corticotropin, as distinct from hydrocortisone, is shown to increase the dehydrogenase activity of microbial cells when pyruvate, isocitrate, oxaloacetate, alpha-ketoglutarate, succinate, furmarate, glucose and beta-oxybutyrate are used as substrates. Hydrocortisone induced a rise of the dehydrogenase activity of microbial cells only in the medium with isocitrate, alpha-ketoglutarate and fumarate, however to a less extent than corticotropin; it lowered this activity in the medium with pyruvate and glucose and did not change it with oxaloacetate, succinate and beta-oxybutyrate. The corticotropin effect is supposed to be extra-adrenal because microbial cells are also subjected to its action.
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PMID:[The effect of corticotropin and hydrocortisone on the dehydration of Krebs cycle substrates in E. coli cells]. 609 2

ACTH and cortisol were measured simultaneously in plasma samples obtained every 5 min from subjects at two different diurnal times. In the first study adrenocorticotropic hormone (ACTH) mean concentration and secretory rate were elevated in anticonvulsant drug-treated temporal lobe epileptic patients in comparison to anticonvulsant drug-treated patients with pseudoseizures. Cortisol mean concentrations and secretory rate were similar in these groups of subjects. In the second study, mean ACTH concentration and secretory rate were higher in temporal lobe epileptic patients than in normal controls. Both measures of ACTH secretion were similar in post-temporal lobectomy patients and normal controls. Mean cortisol concentration and secretory rates were highest in the temporal lobe epileptic patients, lowest in normal controls, and intermediate in post-temporal lobectomy patients. We conclude that ACTH and cortisol secretion is abnormal in temporal lobe epileptic patients. Temporal lobectomy restores abnormal ACTH secretion to normal whether or not seizures are controlled. The absence of ACTH changes in the pseudoseizure patients suggests that these changes are not drug induced. Cortisol secretion is similar in temporal lobe epileptic patients and pseudoseizure patients, suggesting a direct effect of the drugs upon the adrenal cortex.
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PMID:Pituitary and adrenal function in epileptic patients. 609 18

Plasma Cortisol and Beta-Endorphin/Beta-Lipotropin-immunoreactivity concentrations were measured in 51 healthy aged subjects. A direct correlation was found between the plasma concentrations of the two hormones. The data suggest that beta-endorphin/beta-lipotropin is not only released during stress but also in resting conditions.
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PMID:Correlation between beta-endorphin/beta-lipotropin-immunoreactivity and cortisol plasma concentrations. 609 61

Severe symptomatic hypoglycemia (serum glucose level, 24 mg/dL) developed in a 23-year-old, 147.3-cm-tall woman during her late second and third trimesters of pregnancy. Endocrine studies disclosed insulin levels less than 2 microU/mL; growth hormone level less than 3 ng/mL; and cortisol level less than 1 microgram/dL. Hydrocortisone therapy corrected her hypoglycemia, and she was delivered of a healthy female infant. Postpartum, her evaluation included normal thyroid function studies, a normal thyroid-stimulating hormone response to protirelin (thyrotropin-releasing hormone), normal serum and urine gonadotropin levels, normal serum prolactin, normal sella turcica tomograms, and a normal EMI brain scan. Urine 17-hydroxycorticosteroids increased during a four-day cosyntropin infusion, but failed to rise after metyrapone administration. The growth hormone level failed to rise after stimulation with levodopa and propranolol administration. The patient was believed to have idiopathic partial hypopituitarism, with hypoglycemia being due to adrenocorticotropic hormone (ACTH) and growth hormone deficiency and the drain of maternal glucose by the fetus. It is suggested that pregnant women with symptomatic hypoglycemia be treated with glucocorticoids while awaiting the results of their endocrine evaluation.
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PMID:Hypoglycemia in pregnancy. Occurrence due to adrenocorticotropic hormone and growth hormone deficiency. 624 99

Adrenal cells were prepared from non-pregnant (anoestrous) sheep, from ewes at days 50, 100 and 130 of pregnancy and at term, and from animals at 1-5 days post partum. The ability of the cells to respond to adrenocorticotrophin (ACTH1-24), alpha-melanocyte-stimulating hormone (alpha-MSH), or combinations of these peptides has been examined in vitro. There was a progressive rise in the basal output of cortisol during pregnancy and in the absence of adrenocorticotrophin the cortisol output from adrenal cells of late pregnant and post-partum sheep the amount of ACTH required to produce half the maximum output of steroid (ED50) was 8 pg/ml. The ED50 increased in early pregnancy to 112 pg/ml and then fell to < 5 pg/ml between day 100 and term. At term both the stimulation ratio and the absolute increment in cortisol output elicited by a maximal concentration of ACTH were greater than at any other time tested in pregnant or non-pregnant sheep. Cortisol output during pregnancy was not increased by alpha-MSH, although at term the stimulatory effect of ACTH1-24 was partially antagonized by alpha-MSH. These results suggest that there may be an increase in the responsiveness of the maternal adrenal during pregnancy, although the factor(s) responsible remains unknown.
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PMID:Increase in the response to adrenocorticotrophin of isolated maternal adrenal cells from sheep in late pregnancy. 625 84


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