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)

The response to administered adrenocorticotropin (ACTH, Cortrosyn) of 26 heterozygotes (parents of children with adrenal 21-hydroxylase deficiency) and of 14 controls are compared. The mean plasma levels of 4-pregnene-3, 20-dione-17, 21-diol (17-OH progesterone) were significantly greater in the heterozygotes 60 minutes (p less than 0.02) and 90 minutes (p less than 0.05) after stimulation with Cortrosyn than in controls. There is, however, considerable overlap. The results would indicate a partial enzyme deficiency in the parents of diseased subjects. There was no significant difference in the response of plasma cortisol.
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PMID:Identification of heterozygote carriers of congenital adrenal hyperplasia by radioimmunoassay of serum 17-OH progesterone. 85 65

In this paper we assess the qualitative and quantitative differences in adrenal function before and after adrenocorticotropic hormone (ACTH) stimulation between normal weight and overweight precocious pubarche (PP) patients. Twelve of the 22 PP patients had a normal body weight for height with linear growth and bone ages (BAs) that were appropriate for chronological age. The remaining 10 PP patients had body weights which were greater than 120% of ideal weight for height and body mass indices (BMIs), which were more than 125% of the ideal for age and sex. In six overweight patients, linear growth was accelerated and BAs were advanced beyond chronological age. All patients underwent an ACTH stimulation test where they received an intravenous bolus of 250 micrograms Cortrosyn. Blood samples were obtained at 0' and 60' for 17-OHProgesterone (17-OHP), 17-OHPregnenolone (17-OHPG), dehydroepiandrosterone (DHEA), androstenedione (A-dione), and cortisol levels. Results of the baseline and stimulated adrenal hormones in the normal weight children were found to be within reference range for normal Tanner I children. In contrast, two of the 10 overweight children were suspected of having congenital adrenal hyperplasia [one with 21-hydroxylase (21-OHase) deficiency, another with 3-betahydroxysteroid (3 beta ol) deficiency]. These two children were indistinguishable in their linear growth rate and degree of skeletal maturation from the other overweight children. In both patients the BA/chronological age and BA/height age (HA) ratios were within two standard deviations of the mean for the overweight patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Excess weight and precocious pubarche in children: alterations of the adrenocortical hormones. 165 53

Little is known about adrenocortical function after coronary bypass surgery in which moderate to deep hypothermia and cardiopulmonary bypass are used particularly with intraoperative steroid administration. Therefore, we performed a pilot study in which immediately preoperative and 18-hour postoperative serum cortisol levels were determined in eight patients who received 1.0 to 1.5 gm of methylprednisolone intravenously during surgery; postoperative serum cortisol (3 +/- 1 microgram%) levels were lower than preoperative levels (15 +/- 3 microgram%, p less than 0.05). To determine the possible cause of these striking findings, the effects of moderate to profound hypothermia and cardiopulmonary bypass upon adrenocortical functioning were investigated without the influence of intraoperative steroid administration. Serum cortisol and aldosterone levels and their response to adrenocorticotropic hormone (ACTH) (Cortrosyn) were determined before coronary bypass surgery and at various postoperative intervals in seven patients. Postoperative cortisol and aldosterone levels increased markedly over their preoperative values, reaching a maximum at 6 to 12 hours (cortisol 16 +/- 8 vs 63 +/- 23 micrograms%, p less than 0.05, aldosterone 15 +/- 5 vs 51 +/- 22 ng%, p less than 0.05). Adrenal response to ACTH was normal preoperatively, during rewarming from hypothermia, and 18 hours, and 7 days postoperatively. In summary, normal adrenal responsiveness occurs after coronary bypass surgery, in spite of hypothermic cardiopulmonary bypass and the effects of anesthesia, and a single dose of methylprednisolone during surgery is associated with markedly lower serum cortisol levels and prevents the usual adrenal stress response to bypass surgery for at least 18 hours postoperatively.
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PMID:Adrenal function following coronary bypass surgery. 299 Jan 87

A circannual analysis was made of serum cortisol, luteinizing hormone (LH), and testosterone concentrations in the male clouded leopard (Neofelis nebulosa). Group I males (n = 4), maintained in a standardized environment, were bled serially during a regimented anesthesia/electroejaculation episode occurring monthly (beginning in January, ending in December). Additional sampling intervals were conducted under anesthesia only (control, n = 8), anesthesia plus a single adrenocorticotropin hormone challenge (ACTH, Cortrosyn, n = 4), or anesthesia plus a single 25 micrograms injection of gonadotropin-releasing hormone (GnRH, Gonadorelin, n = 4). Group II males (n = 6) from various zoological collections were sampled serially under the same semen collection conditions on one random occasion within the year. Serum cortisol levels were 2 times greater than values measured in comparable studies involving other felid species. Cortisol concentrations were similar during electroejaculation and control (anesthesia only) episodes, and mean levels did not rise as a result of semen collection. Adrenocorticotropin caused an immediate rise in cortisol to levels at least 1.5 times greater than electroejaculated or control counterparts. Mean concentrations of basal cortisol in individual males gradually increased as the year progressed, possibly as a consequence of repeated psychogenic stress. Between seasons, there were no differences in mean LH; however, testosterone levels were greater (p less than 0.05) in the winter compared to all other seasons. There were no differences (p greater than 0.05) between individual males in secretory patterns or mean concentrations of cortisol, LH, or testosterone. Within males, distinct temporal fluctuations were observed in both LH and testosterone during the approximately 80-min sampling interval. Neither LH nor testosterone profiles appeared affected by cortisol patterns during electroejaculation or after an ACTH challenge. A bolus of GnRH induced a marked rise in serum LH and testosterone within 15 and 30 min respectively, indicating that these two hormones were coupled. Both LH and testosterone profiles in Group II males mimicked those in Group I; concentrations of cortisol in Group II males immobilized on one occasion were similar to those of Group I animals sampled from January-May but appeared to be less than values measured from June-December. These data demonstrate that the clouded leopard, compared to other felids, produces markedly elevated concentrations of cortisol, which are likely related to an aggressive behavioral temperament.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Reproductive physiology of the clouded leopard: II. A circannual analysis of adrenal-pituitary-testicular relationships during electroejaculation or after an adrenocorticotropin hormone challenge. 301 73

The effect of administration of a high dose of glucocorticoid (triamcinolone) on serum lipids and lipoproteins was studied in rats. Changes in serum lipids, especially cholesterol, were most marked when 5 mg/kg body weight of triamcinolone was injected daily for 5 days. Serum lipoproteins were separated by ultracentrifugation followed by gel-filtration chromatography. Cholesterol distribution between apolipoprotein B-containing lipoproteins (very-low-density and low-density lipoproteins), high-density lipoprotein1 (HDL1), and HDL2 was determined after administration of triamcinolone with or without additional treatment with adrenocorticotropin (ACTH; Cortrosyn, 6 IU/rat). When triamcinolone was administered, cholesterol concentrations in HDL1 and HDL2 were elevated in a dose-dependent manner, but there was no significant change in apolipoprotein B-containing lipoprotein cholesterol levels. When ACTH was administered in combination with triamcinolone, the concentrations of all serum lipids except triacylglycerol were significantly lowered compared with rats treated with triamcinolone alone. HDL1-cholesterol concentration in serum was significantly (P less than 0.001) lowered from 69 +/- 13 mg/dl (mean +/- S.D.) in triamcinolone-treated rats to 36 +/- 4 mg/dl by the administration of ACTH plus triamcinolone. The additional administration of ACTH in triamcinolone-treated rats caused a slight, but significant, decrease in cholesterol concentration in apolipoprotein B-containing lipoproteins; however, HDL2-cholesterol level was not significantly affected, although there was a tendency for it to be lowered.
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PMID:Glucocorticoid-induced elevation of serum high-density lipoprotein-cholesterol and its reversal by adrenocorticotropin in the rat. 302 35

The effect of stimulating and suppressive influences on plasma aldosterone in normal man and in patients with primary aldosteronism were studied using a sensitive double-isotope derivative assay for aldosterone. In normal sitting subjects, values were 9.2+/-0.9 (SE) mmug/100 ml and in subjects supine for 1 hr plasma aldosterone was 5.2+/-0.4 (SE) mmug/100 ml. Adrenocorticotropic hormone (ACTH), 0.5 U/hr, produced a rise of 46.8+/-22 (SE) mmug which was similar to the 1-hr effect of an infusion of a synthetic ACTH (beta(1-24), Cortrosyn). Angiotensin II in pressor amounts also increased plasma aldosterone 21.5+/-2.9 (SE) without change in plasma cortisol, whereas a subpressor dose ([unk]) had minimal effect.Fludrocortisone, 1.2 mg/day for 3 days, suppressed plasma aldosterone levels to 1.8+/-0.7 (SE) mmug/100 ml in five normal sitting subjects (P < 0.01); however, dexamethasone, 2 mg/day for 1-2 days, did not lower aldosterone concentration in plasma. In six patients with primary aldosteronism, plasma aldosterone on a normal sodium diet was 39.1+/-4.4 (SE) which differed significantly from normal sitting or supine subjects (P < 0.001). In contrast to the normal subjects, neither a pressor infusion of angiotensin II for 1 hr, nor fludrocortisone, 1.2 mg/day for 3 days, impressively altered plasma aldosterone levels. This approach appears to be useful for the study of the acute physiology and control mechanisms of aldosterone production in normal and hypertensive man.
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PMID:Stimulation and suppression of aldosterone in plasma of normal man and in primary aldosteronism. 430 57

Total 24-hour urinary 17-ketosteroid (17-KS) and serum testosterone (T), androstenedione (A), and dehydroepiandrosterone sulfate (DHEA-S) concentrations were measured before and after the administration of Cortrosyn and dexamethasone in 46 hirsute and 18 nonhirsute women. Both the baseline urinary 17-KSs and serum androgen levels were significantly higher (P less than 0.05) in hirsute than in nonhirsute subjects. In 58% of the patients in the hirsute group serum androgen concentrations were found to be elevated, while 17-KS levels in 24-hour urine collections were within normal limits. In 87% of our hirsute subjects at least one serum androgen was elevated. Serum DHEA-S concentration was elevated in almost half of the patients with hirsutism. For the evaluation of hyperandrogenism, measurements of serum androgens give more accurate information to the clinician. Dynamic stimulation-suppression studies do not appear to offer any better understanding of the type of androgens involved or a rational guide to the choice of therapy. Hirsute patients were found to be responding less to corticotropin stimulation in comparison to nonhirsute patients. The stimulation rate was significantly higher in 17-KS, A, T, and DHEA-S concentrations in nonhirsute than in hirsute patients.
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PMID:Hirsutism: diagnostic approach and stimulation-suppression dynamics of androgens in the female. 612 19

Tetracosactide (Synacthen, Ciba) increases the concentration of corticosterone in the aqueous humour of the rabbit eye. The maximal increase, about 5-fold of the basal level, occurs with a slight delay of approximately 30 min after the maximally stimulated corticosterone level in blood plasma. Glucocorticoid elevation is paralleled by an increase of protein content and a slight rise of glucose in aqueous. A disruption of the blood-aqueous barrier by ACTH similar to the action of alpha-melanocyte-stimulating hormone is suggested.
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PMID:Effect of ACTH on the composition of the aqueous humour of the rabbit eye. 631 28

The factors that regulate growth and function of the human adrenal gland during intrauterine development and thereafter are ill defined. Whereas others have reported that adrenocorticotropic hormone (ACTH) augments the inhibitory effect of transforming growth factor-beta (TGF-beta) on growth of fetal zone (FZ) cells of the human fetal adrenal, we recently found that ACTH interferes with TGF-beta's inhibition of growth of fetal adrenal neocortex cells. In this study we sought to assess independently the effects of TGF-beta in the absence and presence of ACTH on growth of FZ cells. TGF-beta, in a time- and dose-dependent manner, inhibited growth (i.e., [3H]thymidine incorporation) of FZ cells. ACTH (Cortrosyn), at 90 pM to 90 nM, was found to interfere with the TGF-beta inhibition of FZ growth. ACTH 1-24 and human ACTH 1-39, both from Sigma Chemical, also were found to blunt the response of FZ cells to TGF-beta. Growth inhibition due to TGF-beta action and the reversal by ACTH of TGF-beta effects on FZ cell growth were confirmed by the results of immunohistochemical analyses of 5'-bromo-2'-deoxyuridine incorporation into nuclei of FZ cells and by indirect evaluations of cell numbers. Both forskolin (10 microM) and dibutyryl adenosine 3',5'-cyclic monophosphate (1 mM), but not phorbol 12-myristate 13-acetate (1 or 100 mM), were able to mimic ACTH actions in blunting the inhibitory effects of TGF-beta on DNA synthesis. We conclude that ACTH, possibly via activation of adenylate cyclase, interferes with, rather than augments, the growth-inhibitory effect of TGF-beta on FZ cell growth.
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PMID:Interactions between TGF-beta and adrenocorticotropin in growth regulation of human adrenal fetal zone cells. 816 71

Prolonged use of glucocorticoids (GCs) can cause prolonged suppression of the hypothalamus-pituitary-adrenal (HPA) axis. This study examined the possibility that corticotropin or its secretagogues such as vasopressin, corticotropin-releasing hormone (CRH), or insulin accelerate recovery of the HPA axis after prolonged treatment with dexamethasone (DEX). Suppression of the HPA axis was induced in rats by DEX at a dosage of 250 micrograms/100 g body weight (BW)/d for 14 days, after which rats were administered saline, corticotropin (Cortrosyn 0.1 mg), ovine CRH (oCRH 6 micrograms), vasopressin (2 U), or insulin (2 U) each morning. Adrenal weight (AW), BW, plasma corticosterone, and corticotropin, as well as pituitary corticotropin content, decreased significantly after DEX treatment. The plasma corticotropin level was significantly elevated 7 days after discontinuation of DEX treatment (day 8) and remained so until day 11, whereas the pituitary corticotropin content had returned to normal on day 8. Plasma corticosterone was suppressed until day 8, but was not significantly different from normal on day 11. The AW was also decreased until day 4, but was not different from normal on day 8 or day 11. The BW of experimental rats remained subnormal during the study period. Treatment of DEX-suppressed rats with exogenous corticotropin induced adrenal hyperplasia, but suppressed the plasma corticotropin level and delayed the normalization of plasma corticosterone until day 11. The insulin-treated group differed in no respect from the saline-treated group. Treatment with oCRH or vasopressin for 8 days normalized plasma and pituitary corticotropin, as well as plasma corticosterone. Hypothalamic immunoreactive CRH (iCRH) did not differ among any treatment groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Corticotropin secretagogues facilitate recovery of the hypothalamus-pituitary-adrenal axis suppressed by prolonged treatment with dexamethasone. 817 41


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