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 systemic activities of methyl 20-dihydroprednisolonate (1), a new local anti-inflammatory steroid synthesized by modifying the 17 beta-ketol side-chain of prednisolone, on pituitary-adrenal function and liver glycogen content were investigated in rats. The parent compound, prednisolone, administered intramuscularly, caused a significant dose-related decrease in plasma levels of corticosterone, adrenocorticotropic hormone (ACTH), and liver glycogen content in rats. In contrast, methyl 20-dihydroprednisolonate caused mild PA suppression and liver glycogen depletion only at high doses. The steroid acid ester did not exert glycogenic activity, unlike prednisolone, in the adrenalectomized rats.
Steroids 1983 May
PMID:Systemic activities of a new anti-inflammatory steroid: methyl 20-dihydroprednisolonate. 631 1

Glucocorticoid-remediable aldosteronism (GRA) is a hereditary cause of human hypertension in which aldosterone secretion is regulated by adrenocorticotropin (ACTH). A genetic mutation which causes GRA has recently been identified in our laboratory, a hybrid or chimeric gene fusing nucleotide sequences of the 11 beta-hydroxylase and aldosterone synthase genes. The finding that these chimeric gene duplications are sensitive and specific markers for GRA allows for a simple, direct genetic test for this disorder. In preliminary studies, we found a wide range of blood pressure levels (including normotension) in affected GRA subjects. Studies to data indicate that this is not related to environmental factors such as sodium intake. Another possibility is that chimeric gene expression is variable, with low blood pressure subjects having reduced gene expression. However, the data have not demonstrated differences in steroid levels in subjects with severe versus mild hypertension. In fact, it is likely that the wide range in blood pressure levels in affected subjects involves interaction of other systems which control blood pressure. Preliminary data in two kindreds suggest that blood pressure levels are reciprocally related to levels of urinary kallikrein excretion, supporting the notion that GRA is a hypertension-predisposing syndrome, with the resultant blood pressure the interaction of the gene mutation with other blood pressure regulatory systems. Although GRA is a mineralocorticoid excess state, as evidenced by profoundly suppressed levels of plasma renin activity, we have observed (contrary to the reported literature) that normokalemia is a typical finding. In one large normokalemic pedigree, preliminary findings indicate that these subjects have a normal capacity to excrete potassium.(ABSTRACT TRUNCATED AT 250 WORDS)
Steroids 1995 Jan
PMID:Glucocorticoid-remediable aldosteronism (GRA): diagnosis, variability of phenotype and regulation of potassium homeostasis. 779 15

Aldosterone production from 11-deoxycorticosterone was stimulated by hemin in primary cultures and homogenates of calf adrenal zona glomerulosa, in a time- and dose-dependent fashion. The ferrochelatase inhibitor 3,5-diethoxycarbonyl-1,4-dihydro-2,4,6-trimethylpyridine (DDC) blocked the stimulation of aldosterone mediated by adrenocorticotropin (ACTH). Addition of hemin after treatment with DDC partially restored ACTH action. These results suggest that hemin may play a role in regulation of aldosterone production.
Steroids 1993 Aug
PMID:Stimulation of aldosterone production by hemin in calf adrenal glomerulosa cell cultures. 821 89

In order to gain a better understanding of adrenal steroid production in guinea pigs, adrenocorticotropin (ACTH) was administered to castrated adult guinea pigs and a series of C-21 and C-19 steroid levels were determined in both adrenals and plasma over a 6-h period. After injection of ACTH, adrenal cortisol and corticosterone concentrations were stimulated by almost 40- and threefold, respectively, whereas the content of C-21 steroid precursors, namely pregnenolone, 17-hydroxypregnenolone, progesterone, and 17-hydroxyprogesterone, was stimulated by two- to 10-fold. Increases of C-19 steroid levels, namely dehydroepiandrosterone (DHEA), androstenedione (4-DIONE), testosterone, and 11 beta-hydroxyandrostenedione (11 beta-DIONE) ranging from 1.5 to eight times were also observed in the adrenals. In castrated guinea pigs, basal plasma DHEA, 4-DIONE, and testosterone levels were undetectable by radioimmunoassay, whereas 11 beta-DIONE concentrations were in a range similar to those in intact animals. In plasma, ACTH had a marked effect on corticosterone, cortisol, and 11 beta-DIONE. The present results indicate that although guinea pig adrenals synthesized several C-19 steroids, only 11 beta-DIONE was secreted by the adrenals into circulation even after administration of ACTH. The biological activity of this hydroxylated C-19 steroid was then assessed by using silastic implants in castrated guinea pigs, and it was shown that plasma 11 beta-DIONE concentrations increased by threefold and had no effect on prostate weight. Moreover, by using ZR-75-1 cells, a mammary cancer cell line extremely sensitive to androgens, we demonstrated that 11 beta-DIONE had an androgenic potency 35-fold less than that of dihydrotestosterone.
Steroids 1993 Jan
PMID:Effects of adrenocorticotropin on adrenal and plasma 11 beta-hydroxyandrostenedione in the guinea pig and determination of its relative androgen potency. 838 68

Using cultured bovine adrenal fasciculata cells (BAC), we investigated the effects of two hormones, corticotropin (ACTH) and angiotensin II (Ang-II) and two growth factors, insulin-like growth factors I (IGF-I) and transforming growth factor beta 1 (TGF beta 1), on the mRNA levels of nuclear proto-oncogenes of the Fos and Jun families and on the mRNA levels of genes expressed in BAC coding for ACTH and AT1 receptors, cytochrome P450scc and P450 17 alpha and 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD). ACTH and IGF-1 increased c-fos and jun-B mRNA levels early with later increases in the levels of mRNA for the ACTH receptor and the three steroidogenic enzymes, and enhanced steroidogenic responses to both ACTH and Ang-II. In contrast, Ang-II increased mRNA coding for the three proto-oncogenes (cfos, c-jun, and jun-B), decreased those for P450 17 alpha and 3 beta-HSD, and caused marked homologous and heterologous steroidogenic desensitization. TGF beta 1 increased only jun-B mRNA and markedly reduced BAC-differentiated functions and steroidogenic responsiveness to both ACTH and Ang-II. The long-term effects of ACTH on human adrenal fasciculata cells were comparable with those observed in BAC, whereas the long term effects of Ang-II and TGF beta 1 were different from those observed in BAC. Whether these species-specific differences are related to a different effect of these factors on proto-oncogene expression is not yet known.
Steroids 1996 Apr
PMID:Regulation of primary response and specific genes in adrenal cells by peptide hormones and growth factors. 873 96

The present study was undertaken to examine the mechanism whereby beta-lipotropin stimulates adrenal steroidogenesis. In guinea pig adrenal cells, beta-lipotropin (10(-8) M) increased basal steroid production 6-, 4-, and 5-fold for cortisol, androstenedione, and dehydroepiandrosterone (DHEA), respectively, whereas the corresponding responses to adrenocorticotropin (ACTH) (10(-9) M) were 12-, 8-, and 7-fold. The conversion of cholesterol to pregnenolone was studied in cells treated with trilostane, an inhibitor of 3 beta-hydroxysteroid delta 4-5 isomerase. beta-Lipotropin (10(-10) and 10(-8) M) and ACTH (10(-9) M) stimulated pregnenolone production in trilostane-treated cells. The production of cortisol and androgens from precursor steroids was also studied in cells treated with aminoglutethimide, an inhibitor of cholesterol side chain cleavage, after addition of exogenous pregnenolone, 17-hydroxypregnenolone, progesterone, or DHEA. Neither ACTH nor beta-lipotropin stimulated cortisol, androstenedione, or DHEA production in the presence of exogenous precursors in aminoglutethimide-treated cells. No inhibition of the beta-lipotropin- or ACTH-stimulated cortisol or androstenedione responses was demonstrated with the opioid receptor antagonist naloxone (10(-11) to 10(-5) M). The results suggest that beta-lipotropin stimulates steroidogenesis by acting on the conversion of cholesterol to pregnenolone and that its effects are not mediated via an opioid receptor but may be mediated via an ACTH receptor.
Steroids 1996 May
PMID:beta-Lipotropin-stimulated adrenal steroid production. 873 40

Anabolic androgenic steroids (AS) have recently been placed on the Food and Drug Administration's (FDA's) list of controlled substances, because of the adverse effects seen in athletes taking accelerated dosages in attempts to enhance performance. Reported deleterious effects on abusers include sterility, gynecomastia in males, acne, balding, psychological changes, and increased risks of heart disease and liver neoplasia. Considering the roles of the immune and neuroendocrine systems and their interactions in many of these pathologies, it is important to determine the effects of these derivitized androgens on this connection. Little is known in this respect. We therefore determined the effects of anabolic steroids on certain immune responses and their effects on the extrapituitary production of corticotropin by lymphocytes. We present evidence that (1) both 17-beta and 17-alpha esterified AS, nandrolone decanoate and oxymethenelone, respectively, significantly inhibited production of antibody to sheep red blood cells in a murine abuse model; (2) the control androgens testosterone and dehydroepian-drosterone (DHEA) or sesame seed oil vehicle had no significant effects on antibody production; (3) nandrolone decanoate and oxymethenelone directly induced the production of the inflammatory cytokines IL-1 beta and TNF-alpha from human peripheral blood lymphocytes but had no effect on IL-2 or IL-10 production; (4) control androgens had no direct cytokine inducing effect; (5) nandrolone decanoate significantly inhibited IFN production in human WISH and murine L-929 cells; and (6) nandrolone decanoate significantly inhibited the production of corticotropin in human peripheral blood lymphocytes following viral infection. These data indicate that high doses of anabolic steroids can have significant effects on immune responses and extrapituitary production of corticotropin. Furthermore, the mouse model should provide an effective means by which to study other deleterious effects of anabolic steroid abuse in humans.
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PMID:Modulation of immune responses by anabolic androgenic steroids. 878 15

The effect of biologically active peptides (adrenocorticotropin, parathyroid hormone, calcitonin, prolactin) and steroids (aldosterone, progesterone, testosterone) hormones on NMR-relaxation proton of tissue water of kidney have been investigated in vitro. Results of this study suggest that peptide hormones caused dehydration of tissues via sodium regulation. Steroids, quite on the contrary, caused the hydration of kidney tissue independent of the movement of osmotic active electrolyte.
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PMID:[Action of biologically active peptides and steroids on nuclear magnetic resonance relaxation of protons of kidney tissue water in vitro]. 929 6

The regulation of the hypothalamo-pituitary-adrenal (HPA) axis in the operative and perioperative period of major surgical procedures is necessary for successful adaption to surgical stress. We report evidence on an altered response of HPA axis regulation in patients who underwent coronary artery bypass grafting (CABG) surgery. Plasma levels of adrenocorticotropin (ACTH), beta-endorphin, and cortisol were determined with radio-immune assay in 50 males for elective CABG surgery. The patients received general anesthesia using a balanced technique with sufentanil, isoflurane, and midazolam. Pre- and intraoperatively, there was no significant increase in plasma cortisol, ACTH, and beta-endorphin levels. On the evening of surgery, all plasma hormone levels were increased. On the evening of the first and second postoperative day, plasma ACTH and beta-endorphin levels returned to the preoperative baseline values. During the same time interval, plasma cortisol levels were significantly elevated and remained high until the end of the study period (p < 0.001). Our results indicate an altered regulation of the HPA axis in the postoperative period of patients after CABG surgery, as they are compatible with similar results in patients after major abdominal surgery, burned patients, and critically ill patients. Therefore, it is assumed that the finding of a postoperative dissociation between ACTH and cortisol is a result of the severity of perioperative adaptive mechanisms rather than of the specific conditions related to cardiac surgery.
Steroids 1997 Nov
PMID:Postoperative dissociation of blood levels of cortisol and adrenocorticotropin after coronary artery bypass grafting surgery. 936 7

The possibility that non-ACTH proopiomelanocortin-derived fragments may stimulate aldosterone production has previously been studied using nonhuman cells with inconsistent results. We have examined the response of aldosterone to beta-endorphin (beta-End) and joining peptide (JP) and compared these with the response to ACTH using eight cell suspensions prepared from human adrenal glands. ACTH, 10(-6), 10(-8), and 10(-10) M, consistently stimulated aldosterone accumulation above that occurring in unstimulated cells (150 +/- 83, 120 +/- 62, and 77 +/- 32 fmol/10(4) cells above basal, respectively; mean +/- SE; p < 0.05). beta-End significantly stimulated aldosterone production at 10(-6) and 10(-8) M (114 +/- 84 and 50 +/- 24 fmol/10(4) cells above basal; p < 0.05); 10(-10) M beta-End did not provide significant stimulation. Furthermore, JP stimulated aldosterone biosynthesis (41 +/- 16 fmol/10(4) cells above basal; p < 0.05), only at the highest concentration used, 10(-6) M. The addition of 10(-8) M ACTH plus 10(-6) and 10(-10) M beta-End to human adrenal cells yielded values significantly greater than those achieved with either agent alone (267 +/- 152 and 183 +/- 89 fmol/10(4) cells above basal; p < 0.05). These data indicate for the first time that beta-End and JP have the capacity to stimulate aldosterone production in human adrenal cells in vitro. The physiological and potential clinical significance of these observations has yet to be elucidated.
Steroids 1998 Sep
PMID:Non-ACTH POMC fragments stimulate aldosterone production by human adrenal cells in vitro. 972 92


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