SEARCH · Search PubMed

Results for “Transcortin”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 541 records · Page 30Linked to original sources

PubMed1975

Aldosterone and renin in essential hypertension.

A review of some recent laboratory findings indicates definite disturbances in aldosterone metabolism and regulation in patients with mild essential hypertension: (a) a significant mean increase in plasma aldosterone concentration in patients with mild and stable essential hypertension, in contrast to the absence of any difference in patients with labile borderline essential hypertension when in a normotensive phase, compared with control subjects; and (b) a significant mean decrease in metabolic clearance rate of aldosterone, associated with a 12% decrease in hepatic blood flow and an increased binding of aldosterone to a transcortin-like plasma globulin. The secretion rate of 18-hydroxy-11-deoxycorticosterone is above the upper range of normal in 60% of patients with mild, uncomplicated essential hypertension. The incidence of low-renin hypertension, when age and race are taken into account, is much lower than previously assumed. Unless measurements are repeated over a long period, one or two low values of plasma renin cannot be considered a permanent marker indicating a special category of patients with essential hypertension. Tonin, a new enzyme discovered by Boucher, which forms angiotensin II directly from a plasma protein, from the tetradecapeptide substrate and from angiotensin I, is present in most tissues, but in highest concentration in the submaxillary gland. This enzyme is under the control of beta-adrenergic receptors.

18-Hydroxydesoxycorticosterone↗

PubMed2000

Clinical diagnosis of hyper- and hypocortisolism.

The clinical correlate of chronic hypercortisolism is Cushing's syndrome (CS). After exclusion of an iatrogenic cause (glucocorticoid administration), two reliable laboratory methods for establishing the diagnosis are (i) measurement of "free" (unmetabolised) cortisol in a 24-hour urine (UFC) sample and (ii) the low-dose (1 or 1.5 mg) dexamethasone (Dex) test. For the latter, Dex is taken orally at midnight, and plasma cortisol is measured at 8 a.m. In normals and in the absence of CS, the morning cortisol (200-650 nmol/L) is suppressed to <80 nmol/L. In endogenous CS of all causes, cortisol suppression by Dex is absent or incomplete. In patients with severe mental depression or stress, suppression may also be incomplete ("false-positives"). However, UFC is normal or only slight increased in the latter group, while it is always markedly increased in clinically apparent CS. In CS, UFC rises proportionally more than plasma cortisol because the cortisol binding plasma protein (transcortin) can bind only about 500 nmol/L cortisol. Protein-bound cortisol is not excreted by the kidney. After establishing the diagnosis CS, the differentiation between its pituitary (ca. 70%), adrenocortical (ca. 20%) or "ectopic" (ACTH production by non-pituitary tumours) (ca. 10%) origin is made by plasma ACTH measurement, a corticotropin releasing hormone injection test (with plasma ACTH/cortisol measurement) and a high-dose Dex (8 mg or more) suppression test. Chronic hypocorticolism can be primary (adrenal disease, Addison's disease) or secondary (pituitary or hypothalamic disorder). UFC measurement is not an established method for confirming hypocortisolism because most analytical methods are too unspecific and insensitive in the subnormal range. Low-normal or subnormal plasma cortisol plus elevated ACTH is the hallmark of Addison's disease. Injection of high doses of ACTH does not lead to a rise in plasma cortisol in these patients. A clearly subnormal cortisol plus low ACTH proves secondary hypocortisolism. Mild forms with low-normal plasma cortisol, however, are more difficult to prove. So-called "dynamic" tests stimulating the whole hypothalamo-pituitary-adrenal axis (insulin hypoglycemia test or metyrapone test) are necessary to confirm the diagnosis. Patients with hypocortisolism, depending on disease severity, must be treated permanently or only in stressful situations with hydrocortisone unless they may die after passing the clinical state of an "adrenal crisis".

Journal Article↗

PubMed1975

Age-related changes in glucocorticoid binding by rat splenic leukocytes: possible cause of altered adaptive responsiveness.

Splenic leukocytes of senescent rats (24-26 mo) exhibit a 60% reduction in cortisol-induced inhibition of 3-H-uridine uptake when compared to mature adult animals (12-14 mo). The degree of inhibition is directly proportional to cortisol dosage up to 2 X 10-6 M. Specific binding of physiological (nanomolar) concentrations of 3-H-cortisol by leukocytic cytosol macromolecules is reduced by over 40% in the older animals. Moreover, Scatchard analyses reveal 60% fewer specific glucocorticoid binding sites in the cytosols of cells from the senescent rats. Such analyses were performed in vitro at 0 C to eliminate metabolism of steroids. In addition, 3-H-dexamethasone was used instead of 3-H-cortisol to eliminate binding to plasma (or serum) transcortin. Inhibition of 3-H-uridine uptake requires specific glucocorticoid binding. The degree of inhibition at varying glucocorticoid dosages is proportional to the amount of specific binding to cytoplasmic macromolecules. Thus, age-related reduction in specific glucocorticoid binding sites may be at least partially responsible for altered responsiveness of splenic leukocytes to these hormones.

Adaptation, Biological↗

PubMed1992

[Interaction of sex steroids with proteins from the soluble fraction of swine and cattle liver (a preliminary analysis)].

The interactions of [3H]estradiol, [3H]testosterone and [3H]progesterone with soluble proteins from porcine and calf liver were studied. The specific binding of [3H]progesterone and [3H]testosterone in calf liver cytosol seems to be due to serum transcortin or its intracellular precursor (analog). Contrariwise, the specific binding of [3H]progesterone observed in porcine liver cytosol was absent in the serum. This binding was characterized by slow association and dissociation dynamics, moderate affinity for the [3H]-ligand and a high binding capacity. The structural determinants of the ligands were studied by competitive inhibition of the [3H]-ligand binding. The delta 4-3-keto group in the steroid A-ring was found to be the most important determinant. An intensive metabolism of [3H]progesterone was observed during its incubation with cytosol (data from thin-layer chromatography). A 3H-metabolite (presumably, 20 beta-dihydroprogesterone) was predominant in the bound ligand fraction. The data obtained suggest that proteins of a steromodulin type are widely distributed in the mammalian liver.

Animals↗

PubMed1975

Binding of glucocorticoid receptors to DNA.

DNA has been implicated as the nuclear acceptor for receptor-glucocorticoid complexes. The present study concerns the interaction of these complexes, isolated from cultured rat hepatoma cells, with purified DNA. This association is rapid, reaching a maximum within a few minutes at 0 degrees, whereas dissociation requires several hours. DNA binds neither free glucocorticoids nor those complexed with transcortin or cytosol proteins different from the receptor. Receptors which are not complexed by steroid have little or no affinity for DNA. "Activation," necessary for the binding of receptor-steroid complexes to isolated nuclei, also enhances DNA binding. The capacity of DNA for binding receptor-steroid complexes is large; saturation was not observed at the complex concentrations studied, using either crude or partially purified receptor preparations. The association of complexes with DNA is inhibited by divalent cations, at increasing ionic strengths, and by mercurial reagents. Complexes bind equally well to bacterial, bacteriophage, or rat DNA; however, there was either no or substantially reduced binding by bacterial 23 S rRNA. The binding of complexes to native DNA is roughly 3-fold greater than to denatured DNA. These characteristics are consistent with the possibility that DNA is the nuclear acceptor for receptor-glucocorticoid complexes; however, the actual composition of the acceptor sites remains unknown.

Animals↗

PubMedDate not supplied

[Effect of furosemide and ACTH on plasma renin, aldosterone and cortisol levels in normal man].

Plasma renin activity (PRA), aldosterone and cortisol's variations are studied in normal salt repleted voluntary men (120 mEq/24 h sodium) before and after furosemide infusion and/or constant infusion of ACTH (beta 1-24 corticotrophin). PRA is determined by angiotensin I radioimmunoassay, plasma aldosterone by specific radioimmunoassay and plasma cortisol by competitive transcortine binding radioassay. 1) PRA and plasma aldosterone increase clearly after acute sodium depletion secundary to furosemide infusion; plasma cortisol increases a little. PRA and aldosterone's variations are identical after endogenous ACTH suppression by dexamethazone administration before study. 2) PRA is not influenced by constant infusion (16 ng/kg/mn) after acute infusion (0.3 mg intravenously) of ACTH (beta 1-24); plasma aldosterone and plasma cortisol increase dramatically and remain constant along the experience. 3) If acute sodium depletion is realized 120 mn after ACTH infusion, PRA still raises; on the other hand plasma aldosterone remains constant. These results confirm that acute sodium depletion stimulates aldosterone secretion by the way of renin angiotensin system then ACTH acts directly on the adrenal cortex. Nevertheless the stimulative action of acute sodium depletion on aldosterone secretion is suppressed by previous acute ACTH stimulation.

Adrenocorticotropic Hormone↗

PubMed1976

Characteristics of progesterone-binding components in neoplastic mammary tissues of the rat.

Characteristics of [3H]progesterone-binding components were studied in cell-free preparations of two hormonally responsive tumors: the R3230AC mammary adenocarcinoma and 9,10-dimethyl-1,2-benzanthracene-induced mammary tumor of the rat. Progesterone-binding macromolecules from cytosols of both mammary neoplasms exhibited sedimentation coefficients of 3.5 to 4.0 S on sucrose gradients of either low or high ionic strength. From Scatchard analyses of titration data, apparent dissociation constants of 4 to 6 X 10(-8) M were determined for ligand-binding protein complexes from either tumor. Specific progesterone-binding capacities varied considerably, ranging from 150 to 650 fmoles/mg of cytosol protein. Optimal binding of [3H]progesterone was reached by 2 to 3 hr at 3 degrees, pH 7.4, and then decreased rapidly. Specificity studies indicated that cortisol, corticosterone, and triamcinolone acetonide competed effectively for [3H]progesterone-binding. This suggested that [3H] progesterone was bound largely to a macromolecule distinct from transcortin, which does not bind glucocorticoids containing 9alpha-fluoro groups. Aldosterone, as well as several androgens and estrogens, were weak competitors of binding except at high concentrations. The nature of the inhibition of progesterone-binding sites by triamcinolone acetonide and corticosterone was competitive. Concurrent titrations of [3H]progesterone and [3H]triamcinolone acetonide-binding sites demonstrated that their binding capacities were similar, considering the relative stabilities of the complexes. These results, which indicated that progesterone and glucocorticoids compete for the same binding site, suggest that these hormones may influence mammary gland differentiation and development by a common mechanism.

9,10-Dimethyl-1,2-benzanthracene↗

PubMedDate not supplied

[Interaction of [3H] corticosterone from blood serum with rat liver cells during aging].

It is shown that the consumption of glucocorticoids from the complexes with serum proteins by hepatocytes decreases with ageing. Transcortin-complexed decrease adenosine monophosphate binding by the liver cells but the degree of this inhibition decreases with an increase of animals' age, which is probably connected with the change in physicochemical properties of steroid-transport blood glycoprotein.

Adenosine Monophosphate↗

PubMed1989

[Effect of estroprogestative drugs on the secretion of corticoadrenal hormones].

Estro-progestative drugs (EPD) have been used for many years and multiple secondary effects have been reported concerning mainly the glucidic and lipidic metabolisms. Effects of EPD on steroid metabolism have also been described and the authors present a review of the literature on this subject. Particularly it appears that EPD affect: the glucocorticoid metabolism, with augmentation of total cortisol although not in its free-form (augmentation of transcortine), the adrenal androgens metabolism, with diminution of their circulating rates, the aldosterone metabolism with augmentation of its secretion. These biological constatations could help explaining some clinical features occurring with administration of EPD: diminution of hirsutism and/or acne, augmentation of body weight, appearance of hypertension.

Adrenal Cortex Hormones↗

PubMed1989

[Current views on the role of disorders of hormonal regulation in the development of altered sensitivity and reactivity of the bronchi].

Altered bronchial sensitivity and reactivity are the basis of different variations of bronchospasm. In addition to exogenous agents, endogenous regulation factors such as adrenal and ovarian hormones are believed to make an important contribution to their development. Asthmatics showed the lowest sensitivity and the highest hyperreactivity to acetylcholine as compared to patients with preasthmatic conditions or chronic bronchitis and healthy consanguins of asthmatic patients. Disturbances of glucocorticoid homeostasis, related to various (adrenal, extra-adrenal (transcortin) and cellular) mechanisms of corticosteroid insufficiency, occurred in the majority of asthmatics and asthmatic bronchitis patients. Identification of various mechanisms of glucocorticoid insufficiency opens up actual approaches to increasing the efficiency of an individual therapy.

Asthma↗

PubMedDate not supplied

[Activity of 5-alpha- and 5-beta-steroid reductases in subcellular liver structures from rats bearing Walker carcinosarcoma].

Change in the activity of cytoplasmic 5 beta- and microsomal 5 alpha-steroid reductases was studied in tumor bearing rats. As shown by thin-layer chromatography conversion of 3H-corticosterone into 5-alpha and 5 beta-dihydro-compounds was decreased 3-fold in rats bearing Walker tumor. Activity of both these enzymes exceeded the initial level 2-3-fold in presence of exogenous NADPH. At the same time, activation of glucose 6-phosphate dehydrogenase was accompanied by simultaneous alteration in content of transcortin-bound corticosterone in rat blood plasma. 5 alpha-reductase was detected in membranes of liver tissue endoplasmic reticulum and in the fraction of free polyribosomes.

Animals↗

PubMed1987

Metabolic effects of two low-dose triphasic oral contraceptives containing ethinyl estradiol and levonorgestrel or gestodene.

A well-known triphasic oral contraceptive (OC) containing ethinyl estradiol (EE) plus levonorgestrel (LNG) was compared with a triphasic containing the same dose of EE in combination with a 14% smaller dose of a new progestogen gestodene (GTD), in a prospective study of 24 and 20 healthy young women, respectively. Serial determinations of lipids, lipoproteins, and carrier proteins, and repeated standardized oral glucose tolerance tests (OGTTs) were conducted during 12 months of OC use. All lipid concentrations recorded before and during both treatments were strictly within the normal range. After 12 months, no significant fluctuations were observed in levels of total cholesterol, HDL-cholesterol, LDL-cholesterol, VLDL-cholesterol, and apolipoprotein A1; concentrations of total triglycerides, phospholipids, and apolipoprotein B were slightly but significantly increased; the epidemiologically important ratios of HDL-cholesterol:total cholesterol and apolipoprotein A1:apolipoprotein B were not significantly changed, while the ratio of LDL-cholesterol:HDL-cholesterol was significantly decreased at 12 months of use of the GTD triphasic. SHBG levels (+ 100% over basal during use of the LNG-OC and + 200% with the GTD-OC) and transcortin (+ 100% over basal) increased early and remained stable. During use of the LNG-OC, glucose tolerance was strictly unchanged, while insulin response to a 75-g glucose load was transiently increased at 6 months (area under the curve [AUC] + 29%) before returning to normal at 12 months. During GTD-OC treatment, glucose tolerance was slightly impaired (AUC + 14%) at 6 months but back to normal at 12 months, while insulin response during OGTT was completely unaltered.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1988

[Pharmacokinetics of prednisolone in children. Study of a correlation with tolerability and therapeutic effect in nephrosis].

In patients with nephrotic syndrome the response to corticosteroids and the way these drugs are tolerated are extremely variable. The purpose of this study was to investigate possible correlations between the pharmacokinetic values of prednisolone and the main clinical criteria of effectiveness and safety. The study was performed on 18 children under corticosteroid therapy: 16 with nephrotic syndrome and 2 with a systemic disease. Measurements were performed by radiocompetition with transcortine after an oral dose of 1 mg/kg bodyweight. Pharmacokinetic values varied considerably, with peak plasma levels ranging from 1.2 to 6.1 micrograms/ml between 20 and 120 minutes, and T 1/2 values of 77 to 648 minutes. Within this scattering of values, some patients were clearly outside the mean T 1/2 value (3.1 +/- 1 hours) due to a particularly fast or slow metabolisation of the drug. In patients with nephrotic syndrome no correlation was found between pharmacokinetic values and criteria of clinical effectiveness, such as the time and dosage required to obtain remissions and the duration of these remissions. Hypoalbuminaemia had no influence on the metabolism of prednisolone. In contrast, there was a correlation between pharmacokinetic values and side-effects, since patients who presented with side-effects also had a significantly greater area under plasma concentration versus time curves. This pharmacokinetic test may be used when corticosteroids produce unusual or unexplainable therapeutic results or adverse reactions.

Child↗

PubMed1988

[Alcohol and endocrinologic homeostasis].

In addition to direct toxic effects on endocrine organs chronic alcohol intake affects regulation of endocrine systems by disturbed liver function. As a result in patients with alcohol-induced liver cirrhosis gonadal axis is characterized by low total and free testosterone, elevated estradiol. LH, FSH, and sexual hormone binding globulin and an enhanced conversion of testosterone to estradiol. Prolactin also is found to be elevated. The thyrotropic axis is characterised by low T3- und T4- as well as elevated rT3-values and normal TSH. STH is elevated, while somatomedin C is decreased. The corticotropic axis may show an abolished circadian rhythm, a negative Dexamethasone-test, low transcortin and elevated free cortisol levels. The disturbance of the calcitropic axis leads to osteoporosis and osteomalacia, due to intestinal hyperparathyroidism and vitamin D malnutrition. In 50% of chronic alcoholics there are elevated insulin and glucagon values and a pathological glucose tolerance test.

Alcoholism↗

PubMedDate not supplied

[Luteal insufficiency and elevation of sex-binding proteins by demegestone].

Demegestone, a norprogesterone derivative, was administered during the luteal phase in 6 normally ovulatory women and in 10 patients with luteal insufficiency. Demegestone decreased the LH surge and the plasma concentrations of estradiol and progesterone in the normally ovulatory women and did not modify the binding capacity of sex steroid binding protein (SBP). In the patients with luteal insufficiency, demegestone increased significantly SBP (0.94 +/- 0.24 vs 1.32 +/- 0.56 micrograms/dl, p less than 0.05) and decreased the free testosterone index (T/SBP) (38.8 +/- 33.3 vs 25.4 +/- 18.5, p less than 0.05). Transcortin, was unchanged during demegestone treatment in both groups of women. The results showed that demegestone did not exercise androgenic activity on SBP conversely to the nortestosterone derivatives which decrease SBP and confirmed that progesterone and norprogesterone derivatives influence positively the regulation of SBP.

Adult↗

PubMed1985

[Interaction of blood sex steroid-binding globulin with cell membranes of human decidual tissue].

The interaction of sex steroid-binding globulin (SHBG) from human blood with plasma membranes of human decidual tissue cells (estradiol target tissue) was investigated. It was shown that SHBG complexed with estradiol specifically interacts with these membranes. The dissociation constant (Kdis) for this interaction is (3.5 +/- 2.0) X 10(-12) M. The interaction of the SHBG-estradiol complex with the membranes is characterized by a high selectivity; such serum globulins as albumin, orosomucoid, transferrin, transcortin and the thyroxine-binding globulin do not compete with SHBG for the binding sites on the membranes. The SHBG-testosterone complex and SHBG alone do not interact with the membranes either.

Binding, Competitive↗

PubMed1977

[Binding of corticosteroids to plasma proteins in the adult green frog, in various physiological conditions].

Binding of corticosterone and aldosterone to plasma proteins of the edible Frog was studied by equilibrium dialysis technique. A high-affinity, transcortin-like, corticosterone binding system has been demonstrated, but, in vivo, the unbound fraction of this corticosteroid is higher that the bound one. Hypophysectomy and thyroidectomy do not change corticosteroids binding parameters which are modified by a variation of temperature.

Aldosterone↗

PubMed1981

[Glucocorticoid receptors and metabolic disorders of the liver and heart following immobilization].

A model of the immobilization stress aided to study the main characteristics of dexametasone-binding and transcortin-like receptors in the liver and heart cytosol, the level of endogenous corticosterone, induction of the glucocorticoid--dependent liver enzyme tyrosine aminotransferase (TATF), and amount of a number of metabolites. The study revealed disturbances of the receptor binding and cellular metabolism during the stress. A sharp increase of endogenous glucocorticoids in blood and tissues along with inhibition of the glucocorticoid receptor binding in organs and of the TATF activity, exhaustion of cellular contents of glucose and cholesterine, a decrease in the protein amount, increasing level of urine in blood and tissues as well as a considerable hyposodiumemia indicate transition of the stress from the compensated phase into the decompensated one.

Animals↗