Search Results
Search for other papers by CONSTANCE de COURCY in
Google Scholar
PubMed
Search for other papers by C. H. GRAY in
Google Scholar
PubMed
1. The reducing method of Talbot, Saltzman, Wixom & Wolfe [1945], and the formaldehyde method of Corcoran & Page [1948], as well as a modification of that of Daughaday, Jaffe & Williams [1948] for the estimation of urinary corticosteroids, have been critically examined.
2. A study has been made of the distribution of reducing material, of formaldehydogenic material and of reducing and Δ4-3-ketosteroids, in the various fractions obtained during the various purification procedures applied to the crude CHCl3 extract.
3. Caustic soda washing does not remove significant quantities of the steroids investigated, although non-steroid reducing and uncharacterized formaldehydogenic material is removed.
4. The water fraction of the benzene-water partition contains all the reducing and Δ4-3-ketosteroids so far detected in urine.
5. The formaldehydogenic method of Corcoran & Page gives slightly higher results than the modified method of Daughaday et al.
6. The acid hydrolysis curves obtained with the Talbot method resembled those described by Paterson, Cox & Marrian [1950], but no regular form of hydrolysis curve was obtained when either formaldehydogenic method was used.
7. A comparison of normal values obtained by the authors using the chemical and paper chromatography techniques revealed that the formaldehydogenic methods estimate a very high proportion of uncharacterized material, whereas results by the reducing method of Talbot et al. approximate relatively closely to those obtained by semiquantitative paper chromatography.
Search for other papers by R. Fraser in
Google Scholar
PubMed
In some fields of steroid endocrinology, it has long been accepted that the potency of a hormone may depend not only on its secretion rate and rate of hepatic clearance but also on specific metabolic transformation at the site of the target cell. The crucial role of tissue 5α reductase activity on the action of testosterone is a spectacular example (Peterson, ImperatoMcGinley, Gautier & Sturla, 1977). Curiously—it is easy to be wise after the event—this line of thought seems rarely to have been exercized in explanations of corticosteroid action. Clearly, the severity of diseases of corticosteroid excess, of which Cushing's and Conn's syndromes are the best known examples, is strongly correlated with the secretion rate of cortisol and aldosterone respectively. However, in some forms of hypertension where deranged corticosteroid action might be expected to provide an acceptable explanation (e.g. increased mineralocorticoid secretion in low-renin essential hypertension), no abnormalities of secretion
Search for other papers by R Vettor in
Google Scholar
PubMed
Search for other papers by C Macor in
Google Scholar
PubMed
Search for other papers by F Novo in
Google Scholar
PubMed
Search for other papers by C Gottardo in
Google Scholar
PubMed
Search for other papers by S Zovato in
Google Scholar
PubMed
Search for other papers by M Simoncini in
Google Scholar
PubMed
Search for other papers by G Federspil in
Google Scholar
PubMed
Search for other papers by D Armanini in
Google Scholar
PubMed
Abnormalities of the hypothalamus-pituitary-adrenal axis and hypersensitivity to corticosteroids have been suggested as major determinants of the development of visceral obesity. Since at the cellular level most effects of corticosteroids are mediated by specific receptors, we evaluated the number of type I and type II corticosteroid receptors in mononuclear leucocytes of 26 obese and 13 control subjects. We also studied the relationship between corticosteroid receptors, measured by radioreceptor assay, and abdominal visceral fat, evaluated by computed tomography scan, plasma and urine corticosteroid hormone concentrations and overall glucose metabolism, assessed by euglycaemic-hyperinsulinaemic clamp. We observed a decrease in type II receptors in the obese subjects (1746 +/- 160 vs 2829 +/- 201 per cell; P < 0.0001), with no change in type I receptors. Type II receptors decreased in relation to body mass index (r = -0.53; P < 0.005) and total glucose disposal (r = 0.51; P < 0.01). Abdominal visceral fat did not correlate with type II receptor number, but did correlate with total glucose disposal (r = -0.35; P < 0.05); the rate of glucose disposal was lower in obese subjects (3.3 +/- 0.3 vs 7.4 +/- 0.4 mg/kg per min; P < 0.001). Plasma and urine cortisol did not differ between the two groups. However, a direct correlation between type II receptor number and both plasma (r = 0.43; P < 0.02) and urine cortisol concentrations (r = 0.60; P < 0.05) was observed. In conclusion, the number of type II corticosteroid receptors in mononuclear leucocytes was found to be lower in obese subjects. This abnormality appears to be related to the degree of adiposity and to the main endocrine-metabolic features of the obesity syndrome, further supporting the hypothesis of involvement of hypothalamus-pituitary-adrenal axis hyperactivity in the pathophysiology of obesity.
Search for other papers by D. EXLEY in
Google Scholar
PubMed
Search for other papers by J. K. NORYMBERSKI in
Google Scholar
PubMed
SUMMARY
An analytical method was developed which comprises the following successive operations: enzymic hydrolysis of urinary steroid conjugates; extraction and initial purification; reduction with potassium borohydride; paper-chromatographic separation into three fractions containing corticosteroid triols, tetrols and pentols, respectively; measurement of 17-hydroxycorticosteroids and of 17-deoxycorticosteroids in each fraction. Subject to certain qualifications the outlined procedure is believed to account separately for the metabolites of cortisol, 17α-hydroxyprogesterone, corticosterone and 11-deoxycorticosterone; it fails to distinguish between the metabolites of 21-deoxycortisol and 11-deoxycortisol.
Assays of urines from non-pregnant women, pregnant women and newborn children revealed a different pattern in the composition of urinary corticosteroids in each group of subjects.
Search for other papers by K. D. R. SETCHELL in
Google Scholar
PubMed
Search for other papers by C. H. L. SHACKLETON in
Google Scholar
PubMed
Search for other papers by R. L. HIMSWORTH in
Google Scholar
PubMed
SUMMARY
The physiological regulation of the plasma corticosteroid concentration, measured by competitive protein-binding, was studied in female rhesus monkeys (M. mulatta) sedated with phencyclidine hydrochloride. Morning basal levels of plasma corticosteroids were found to be in the range 8·0–25·2 μg/100 ml, which is lower than that previously reported in this species. A circadian rhythm in plasma cortisol concentration was demonstrated. Prolonged sedation with phencyclidine was associated with a gradual increase in the plasma cortisol concentration. Synthetic α1–24 adrenocorticotrophic hormone given intravenously caused a rapid rise in plasma cortisol, the minimum effective dose was between 1 and 10 ng/kg body weight and the response was maximal after 1000 ng/kg. The administration of lysinevasopressin and the induction of hypoglycaemia by insulin were both followed by an increase in the plasma corticosteroid concentration. Metyrapone caused a decline in plasma 11-hydroxycorticosteroids and a concomitant increase in total corticosteroids measured by competitive protein-binding. It is concluded that the hypothalamic-pituitary-adrenal system in the rhesus monkey functions in a manner which is qualitatively and quantitatively similar to that of man.
Search for other papers by A. CHADWICK in
Google Scholar
PubMed
SUMMARY
The lactogenic effect of adrenocorticotrophin (ACTH) injected into pseudopregnant rabbits has been confirmed. A synthetic partial ACTH peptide (Synacthen) was also lactogenic. The sensitivity to local lactogenic stimuli of the mammary glands of ACTH-treated rabbits and rabbits treated with corticosteroids was greater than that in untreated rabbits. The findings are discussed in relation to the factors controlling lactogenesis.
Division of Clinical Developmental Sciences, Academic Section of Obstetrics and Gynaecology, Centre for Developmental and Endocrine Signalling, St George’s University of London, Cranmer Terrace, London SW17 0RE, UK
Search for other papers by L M Thurston in
Google Scholar
PubMed
Division of Clinical Developmental Sciences, Academic Section of Obstetrics and Gynaecology, Centre for Developmental and Endocrine Signalling, St George’s University of London, Cranmer Terrace, London SW17 0RE, UK
Search for other papers by D R E Abayasekara in
Google Scholar
PubMed
Division of Clinical Developmental Sciences, Academic Section of Obstetrics and Gynaecology, Centre for Developmental and Endocrine Signalling, St George’s University of London, Cranmer Terrace, London SW17 0RE, UK
Search for other papers by A E Michael in
Google Scholar
PubMed
least in part, to displacement of cortisol from corticosteroid-binding globulin by progesterone ( Andersen 1990 ). It has been proposed that this periovulatory rise in ovarian glucocorticoids may directly influence the oocyte quality and control the
Search for other papers by A. J. BRADLEY in
Google Scholar
PubMed
Search for other papers by I. R. McDONALD in
Google Scholar
PubMed
Search for other papers by A. K. LEE in
Google Scholar
PubMed
Departments of Physiology and *Zoology, Monash University, Clayton, Victoria, Australia
(Received 24 February 1976)
In natural populations of the shrew-like marsupial Antechinus stuartii all the males die within 3 weeks of the beginning of a single mating period in late winter. Males captured before this period begins and caged singly survive well beyond the time of natural mortality. During the mating period the males become extremely aggressive; vagrancy and interactions increase greatly and copulatory activity is frequent and prolonged (Woolley, 1966, Wood, 1970; Braithwaite, 1974). This is associated with evidence of increased adrenocortical activity (Barnett, 1973). Administration of cortisol to males captured and caged singly before the breeding period causes a significant dose-related mortality (Bradley, McDonald & Lee, 1975). However, the mortality is only 45% even when the plasma total corticosteroid concentration is well above the natural breeding level. Also, the plasma corticosteroid concentration of females in natural populations is
Search for other papers by R. J. HEITZMAN in
Google Scholar
PubMed
Search for other papers by T. C. ADAMS in
Google Scholar
PubMed
Search for other papers by G. D. HUNTER in
Google Scholar
PubMed
17α-Hydroxycorticosterone (F) and corticosterone (B) are the two most abundant steroids in bovine adrenal venous blood (Bush, 1953). The competitive protein-binding assay of Bassett & Hinks (1969) is equally sensitive for both these steroids. This fortuitous advantage, together with the need for only small volumes of blood (< 5 ml.), makes this method of assay ideal for the determination of bovine peripheral plasma corticosteroids.
Ayrshire or Friesian cows, kept under cover and accustomed to being handled, were fed on a diet normal for the Institute herd. A list of the different groups of cows is given in Table 1. All blood samples were taken between 14.00 and 15.00 hr. The sample (about 5 ml.) was taken, on to heparin, from the jugular vein within 30 sec. of approaching the animal. After centrifugation, plasma was stored at −15° until required.
The assay of plasma corticosteroids was essentially as described by Bassett
Search for other papers by N. Jenkins in
Google Scholar
PubMed
Search for other papers by J.D. Ellison in
Google Scholar
PubMed
ABSTRACT
Bovine FSH stimulated a six fold increase in secretion of plasminogen activator by immature bovine Sertoli cells with half-maximum response (ED50) at 145ng/ml. Treatment with FSH and either dexamethasone, cortisol or corticosterone produced a dose-dependent suppression of PA activity, with ED50 values of 35, 320 and >650nmol/l respectively. Effects of dexamethasone required over 6 h incubation to become significant (P < 0.001), and were blocked by inhibitors of RNA synthesis and translation. These data demonstrate direct effects of corticosteroids on Sertoli cells, resulting in the synthesis of antiprotease factors which antagonize the actions of FSH.
