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)

These experiments were designed to test for interactions between dose and time of administration of steroids in control of adrenocorticotropin hormone (ACTH). Five dogs were infused for 30 min with cortisol and corticosterone in a 2:1 ratio at a total rate of 1.5 or 3.0 micrograms.kg-1.min-1 beginning 120, 90, 60, 30, or 0 min before injection of insulin (0.5 U/kg). The infusions increased total plasma corticosteroids to approximately 50 or 80 ng/ml. Inhibition of basal ACTH occurred when infusion of steroid at either rate began greater than or equal to 60 min earlier. The degree of inhibition of stimulated ACTH was dependent on both steroid dose and timing of steroid infusion relative to the stimulus. Increasing corticosteroids to 50 ng/ml reduced the ACTH response to hypoglycemia if the infusion began 30 min, but not 60, 90, or 120 min earlier. Increasing corticosteroids to 80 ng/ml inhibited the response if the infusion began 120 or 60 min before injection of insulin. The data suggest that 1) inhibition of stimulated ACTH required less than or equal to 30 min to appear; 2) the duration of corticosteroid feedback is steroid-dose related; 3) basal ACTH secretion is more sensitive than stimulated ACTH to steroid inhibition; 4) small increments in plasma corticosteroids over short periods of time can inhibit canine ACTH.
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PMID:Control of canine ACTH by corticosteroids: interaction between dose and time. 282 28

Synthetic ovine corticotropin-releasing hormone (oCRH) is a potent and specific ACTH secretagogue in man. Threshold and maximal i.v. doses are 0.01-0.03 and 3-10 micrograms/kg or less, but increase in frequency, severity, and duration at higher doses. oCRH produces a biphasic plasma immunoreactive (IR)-ACTH response and has a prolonged duration of action that is probably due to its long circulating half-life. Other pro-opiomelanocortin IR-peptide are secreted concomitantly in equimolar amounts. Plasma IR-cortisol concentration tends to follow that of ACTH, but also reflects cortisol's longer circulating half-life and the fact that acutely the maximally-stimulating plasma IR-ACTH level is about 45 pg/ml. oCRH is as effective given s.c. as i.v., but intranasal administration is only 1% as effective. Sex and age have no effect on the plasma IR-ACTH and IR-cortisol responses to oCRH. The time of day of oCRH administration has little influence on the plasma IR-ACTH response, but the plasma IR-cortisol response is much greater to oCRH given later in the day than early in the morning. Plasma IR-ACTH response to oCRH is more dependent on the basal plasma IR-cortisol level than the time of day. Arginine vasopressin given at the same time as oCRH potentiates 4-fold the plasma IR-ACTH response to oCRH alone, almost to levels obtained with insulin-induced hypoglycemia. However, oCRH administered at the onset of insulin-induced hypoglycemia does not cause higher plasma IR-ACTH levels, indicating that endogenous CRH levels are maximally-stimulating during the hypoglycemic response.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Corticotropin-releasing hormone: stimulation of ACTH secretion in normal man. 283 99

The records of 72 pediatric and adolescent patients with multiple hypothalamic and/or pituitary hormone deficiencies of nontumoral origin who were followed up for years and receiving somatotropin, thyroxine, and sex hormones at the appropriate age have been reviewed. According to their corticotropin-releasing factor-corticotropin-cortisol (CAC) axis function as evaluated by basal plasma cortisol levels and the response of cortisol to insulin hypoglycemia and to corticotropin-releasing factor, the patients were divided into three groups: group 1 (n = 25), patients with multiple hypothalamic and/or pituitary hormone deficiencies with normal CAC axis; group 2 (n = 38), patients with partial CAC deficiency without cortisol replacement therapy (hydrocortisone); and group 3 (n = 9), patients with CAC deficiency receiving hydrocortisone therapy (5 to 10 mg/d). Repeated CAC axis evaluation in patients of group 2 over years revealed a progressive decrease in the basal and stimulated cortisol levels with age and pubertal advancement. Despite the low cortisol levels and the low cortisol response to insulin hypoglycemia, these patients did not have clinical symptoms until the end of puberty when nine of 24 patients complained of abdominal pain, weakness, or anorexia. Linear growth, which was followed up in all patients at regular intervals, showed a lower growth velocity and irregular growth in response to somatotropin treatment in the patients receiving low doses of hydrocortisone (group 3 patients when compared with group 2 patients not receiving hydrocortisone).
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PMID:When should hydrocortisone therapy be instituted in children with hypopituitarism? 283 78

These experiments were designed to determine whether stimulated adrenocorticotropic hormone (ACTH) secretion in dogs can be rapidly inhibited by increases in plasma corticosteroid concentrations. Five dogs were injected with a 2:1 mixture of cortisol to corticosterone (corticosteroids; total doses of 22.5, 45, or 90 micrograms/kg) or vehicle simultaneously with the injection of insulin (0.5 U/kg). These dogs were also injected with corticosteroids (45 micrograms/kg) with ovine corticotropin-releasing factor (oCRF-41; 1 micrograms/kg) or with the same dose of corticosteroids alone. Plasma ACTH and corticosteroid concentrations were measured for 90 min after the injections. The inhibition of ACTH secretion was significant 10 min after injection of oCRF-41 and 40 min after injection of insulin. The first significant increase in ACTH during insulin-induced hypoglycemia does not occur until 30 min, however. Therefore, after both of these stimuli to ACTH, the ACTH response is inhibited within approximately 10 min of its onset. The results suggest that canine ACTH responses to stimuli can be rapidly inhibited and that one site of this inhibition is the pituitary.
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PMID:Evidence for rapid inhibition of ACTH by corticosteroids in dogs. 284 78

We infused submaximal feedback doses of either dexamethasone (DEX; 0.1 microgram.kg-1.min-1) or corticosterone and cortisol (B+F; 1.5 micrograms.kg-1.min-1) intravenously for 40 min into conscious dogs and measured the adrenocorticotropic hormone (ACTH) responses to hypoglycemia induced by insulin (0.1 U/kg) or to ovine corticotropin-releasing factor (oCRF; 1 microgram/kg); both agents were injected at 120 min. The dose of DEX was chosen to produce suppression of the ACTH response to oCRF equivalent to that produced by B+F. The purpose of the study was to determine 1) whether CRF- and hypoglycemia-induced ACTH secretion are equally inhibited by glucocorticoid treatment and 2) whether DEX and B+F have differential effects in the inhibition of stress-induced ACTH secretion. We found that peak ACTH responses to hypoglycemia and CRF were equally inhibited by DEX (36 +/- 6 and 52 +/- 9%, respectively). The peak ACTH responses to hypoglycemia and CRF were also equally inhibited after B+F infusion (45 +/- 13 and 65 +/- 5%, respectively). There was no significant interaction between the steroid administered and the stimulus given in controlling the ACTH response (by 2-way analysis of variance). The results suggest that pituitary feedback is of primary importance in suppression of canine ACTH secretion by delayed feedback and that the natural and synthetic steroids both act at this site.
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PMID:Steroid inhibition of canine ACTH: in vivo evidence for feedback at the corticotrope. 284 95

A 45-year-old man with type I diabetes mellitus of 25-yr duration and well controlled by conventional insulin therapy developed an isolated adrenocorticotropic hormone (ACTH) deficiency. He presented with a 3-month history of weight loss, weakness, anorexia and persistent tendency to hypoglycemia that he had never experienced before. Basal and dynamic endocrine testing disclosed absent cortisol secretion caused by an isolated ACTH deficiency due to a primary pituitary defect. Corticosteroid replacement therapy allowed again a good glycometabolic control. The possible causes of hypoglycemia in insulin-treated diabetes and the pathogenetic basis of the reported association are discussed.
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PMID:Development of isolated ACTH deficiency in a man with type I diabetes mellitus. 284 79

The response of plasma immunoreactive (IR)-ACTH, IR-beta-endorphin (beta-END) and IR-cortisol to insulin-induced hypoglycaemia, an acute stimulus to the pituitary corticotrophs through the central nervous system, and to synthetic ovine corticotrophin-releasing hormone (CRH), a direct corticotroph stimulator, were studied in normal males and males with myotonic dystrophy. Myotonics had an increased IR-ACTH and IR-beta-END response to hypoglycaemia and an increased IR-ACTH response to CRH compared with normals. Plasma IR-cortisol response were not different in either group of subjects to both stimuli. This neuroendocrine abnormality in myotonic dystrophy may represent a manifestation of the purported specific cell membrane defect underlying the disease. This is the first report of an abnormality in proopiomelanocortin peptide release in myotonic dystrophy.
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PMID:Increased pro-opiomelanocortin-derived peptide release in myotonic dystrophy. 284 97

This study was designed to assess effects of insulin-induced hypoglycemia on plasma and cerebrospinal fluid (CSF) levels of immunoreactive (ir) beta-endorphins, adrenocorticotropin (ACTH), cortisol, norepinephrine, insulin, and glucose in the conscious, overnight fasted dog. Dogs received either an intravenous infusion of saline or insulin (5 mU/kg/min) for 3 h. Infusion of saline alone in conjunction with acute sampling of CSF caused no measurable perturbations of glucose homeostasis. Insulin infusion caused a 60% drop in both plasma and CSF glucose. Plasma levels of ir-beta-endorphins, ACTH and cortisol rose markedly. CSF levels of ir-beta-endorphins and ACTH also increased. While the magnitude of the increase was smaller than that in the plasma, it was greater than would be expected if crossover of the peptides from the plasma were the sole source of the increase. Hypoglycemia also induced elevations in CSF cortisol and insulin. In addition, there was a 45% decrease in CSF norepinephrine in spite of large elevations of norepinephrine in the plasma. We conclude that hypoglycemia is associated with marked changes in central as well as peripheral levels of neuroendocrine factors. The importance of these changes in mediating acute and long-term responses to hypoglycemia remains to be established.
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PMID:Effects of insulin-induced hypoglycemia on plasma and cerebrospinal fluid levels of ir-beta-endorphins, ACTH, cortisol, norepinephrine, insulin and glucose in the conscious dog. 285 80

The response of the sympathoadrenal system to hypoglycaemia of different etiology was studied in seven infants, aged 10-189 days. Five infants had hyperinsulinism secondary to nesidioblastosis or to a beta-cell adenoma of the pancreas, one infant had neonatal sepsis due to staphylococcal infection and one infant congenital growth hormone (HGH) and adrenocorticotropic hormone (ACTH) deficiency. In babies with hyperinsulinism, plasma noradrenaline increased from 0.29 +/- 0.03 to 0.61 +/- 0.09 ng/ml (P less than 0.01), whereas adrenaline increased only in three, but did not change in two babies. Increases in heart rate and blood pressure paralleled these changes. In hypoglycaemia due to congenital sepsis, noradrenaline increased from 0.39 to 1.64 ng/ml and adrenaline from 0.05 to 0.86 ng/ml. This was associated with marked haemodynamic changes. In congenital HGH and ACTH deficiency, the low basal plasma levels of noradrenaline (0.12 ng/ml) and adrenaline (0.01 ng/ml) remained unchanged in response to hypoglycaemia. Heart rate and blood pressure were unaffected. The sympathoadrenal system was activated by hypoglycaemia in all infants except in congenital HGH and ACTH deficiency. In contrast to adults, noradrenaline was the preferentially released catecholamine, suggesting an involvement of noradrenaline in glucose counter regulation in infancy.
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PMID:Sympatho-adrenal response to hypoglycaemia in infants. 285 Sep 15

Acute insulin-induced hypoglycaemia in humans provokes autonomic neural activation and counterregulatory hormonal secretion mediated in part via hypothalamic stimulation. Many patients with Type 1 (insulin-dependent) diabetes have acquired deficiencies of counterregulatory hormonal release following hypoglycaemia. To study the integrity of the hypothalamic-pituitary and the sympatho-adrenal systems, the responses of pituitary hormones, beta-endorphin, glucagon and adrenaline to acute insulin-induced hypoglycaemia (0.2 units/kg) were examined in 16 patients with Type 1 diabetes who did not have autonomic neuropathy. To examine the effect of duration of diabetes these patients were subdivided into two groups (Group 1: 8 patients less than 5 years duration; Group 2: 8 patients greater than 15 years duration) and were compared with 8 normal volunteers (Group 3). The severity and time of onset of hypoglycaemia were similar in all 3 groups, but mean blood glucose recovery was slower in the diabetic groups (p less than 0.01). The mean responses of glucagon, adrenaline, adrenocorticotrophic hormone, prolactin and beta-endorphin were similar in all 3 groups, but the mean responses of growth hormone were lower in both diabetic groups than in the normal group (p less than 0.05). The mean increments of glucagon and adrenaline in the diabetic groups were lower than the normal group, but these differences did not achieve significance; glucagon secretion was preserved in several diabetic patients irrespective of duration of disease. Various hormonal responses to hypoglycaemia were absent or diminished in individual diabetic patients, and multiple hormonal deficiencies could be implicated in delaying blood glucose recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Counterregulatory hormonal responses to hypoglycaemia in type 1 (insulin-dependent) diabetes: evidence for diminished hypothalamic-pituitary hormonal secretion. 285 69


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