Effects of the Glucocorticoid Antagonist RU 486 on Pituitary-Adrenal Function in Patients with Anorexia nervosa and Healthy Volunteers: Enhancement of Plasma ACTH and Cortisol Secretion in Underweight Patients

1993 ◽  
Vol 57 (6) ◽  
pp. 1082-1091 ◽  
Author(s):  
Mitchel A. Kling ◽  
Mark A. Demitrack ◽  
Harvey J. Whitfield, Jr. ◽  
Konstantine T. Kalogeras ◽  
Samuel J. Listwak ◽  
...  
1962 ◽  
Vol 25 (2) ◽  
pp. 199-209 ◽  
Author(s):  
V. WYNN ◽  
J. LANDON ◽  
V. H. T. JAMES

SUMMARY The effect of methandienone administration on urinary steroid excretion has been studied in subjects with normal pituitary-adrenal function and in patients with various endocrine diseases. In the control subjects, a marked suppression of urinary 17-KS and 17-OHCS excretion occurred, which persisted throughout even prolonged periods of methandienone administration. Upon cessation of methandienone treatment a prompt rise in urinary steroid excretion occurred, on occasions to levels slightly higher than those seen before treatment. Similar results were obtained in subjects with acromegaly and Cushing's syndrome, but in patients with anorexia nervosa and a low basal steroid excretion, the suppressive effect of methandienone was less marked. During treatment with methandienone, pituitary response to metopirone was depressed, but adrenal response to corticotrophin was unaltered. It was concluded that methandienone diminishes the rate of production of adrenocortical steroid by inhibiting corticotrophin production or release. Unlike the inhibition observed during treatment with glucocorticoids, it was not associated with atrophy of the adrenal glands.


1986 ◽  
Vol 314 (21) ◽  
pp. 1335-1342 ◽  
Author(s):  
Philip W. Gold ◽  
Harry Gwirtsman ◽  
Peter C. Avgerinos ◽  
Lynnette K. Nieman ◽  
William T. Gallucci ◽  
...  

2008 ◽  
Vol 93 (11) ◽  
pp. 4418-4421 ◽  
Author(s):  
Palmiero Monteleone ◽  
Cristina Serritella ◽  
Vassilis Martiadis ◽  
Pasquale Scognamiglio ◽  
Mario Maj

Introduction: Peptides of the gut-brain axis have a pivotal role in the regulation of energy homeostasis. Obestatin, a sibling of ghrelin derived from preproghrelin, is thought to oppose ghrelin effects on food intake. Because changes in ghrelin levels have been associated with anorexia nervosa (AN) and bulimia nervosa (BN), the investigation of obestatin production may further contribute to understanding the role of peripheral peptides in patients with eating disorders. Methods: In the present study, we measured circulating blood levels of obestatin and ghrelin and assessed their relationships with anthropometric and clinical measures in 20 AN patients, 21 BN patients, and 20 appropriate healthy controls. Results: Compared with healthy women, patients with BN showed no significant differences in plasma obestatin and ghrelin concentrations and in the ghrelin/obestatin ratio, whereas underweight AN patients displayed significantly increased circulating levels of both obestatin (P < 0.009) and ghrelin (P < 0.002) and an increased ghrelin/obestatin ratio (P < 0.04). Moreover, in AN women, positive correlations emerged between the ghrelin/obestatin ratio and current body weight and body mass index. Conclusions: Underweight AN patients are characterized by increased concentrations of ghrelin and obestatin and a higher ghrelin to obestatin ratio. No changes in circulating ghrelin or obestatin as well as in ghrelin to obestatin ratio seem to occur in acutely ill patients with BN. Although those changes likely reflect the physiological state of symptomatic AN individuals, they may also contribute to the pathophysiology of the disorder.


1985 ◽  
Vol 108 (2) ◽  
pp. 261-265 ◽  
Author(s):  
V. Coiro ◽  
P. Chiodera ◽  
G. Rossi ◽  
R. Volpi ◽  
M. Salvi ◽  
...  

Abstract. iv administration of oxytocin decreases plasma ACTH-cortisol levels in normal men. In contrast, naloxone, a specific opioid antagonist, stimulates cortisol release, suggesting that opioid peptides exert an inhibitory control on ACTH-cortisol secretion. The present study was carried out in an attempt to determine whether an opioid pathway mediates oxytocin action; therefore, we evaluated the effect of naloxone on the decrease of cortisol induced by oxytocin. Six normal men were treated iv with oxytocin (2 IU as a bolus), naloxone (4 mg as a bolus plus 10 mg infused for 2 h) or a combination of the 2 drugs. Plasma cortisol levels were determined in samples taken before and 2 h after drug treatment. As expected, administration of oxytocin significantly decreased cortisol secretion, while naloxone had a stimulatory effect on plasma cortisol levels. When oxytocin injection was followed by administration of naloxone, cortisol levels remained unchanged; thus, naloxone abolished a cortisol decrement in response to oxytocin. These findings show that in man oxytocin requires an active opioid system in order to produce its inhibitory action on ACTH-cortisol secretion, suggesting that this effect of oxytocin could be mediated by an opioid pathway.


1985 ◽  
Vol 110 (3) ◽  
pp. 289-295 ◽  
Author(s):  
Hans-Udo Schweikert ◽  
Horst Lorenz Fehm ◽  
Rudolf Fahlbusch ◽  
Rainer Martin ◽  
Rainer Kolloch ◽  
...  

Abstract. A 55 year old woman with an unusual form of Cushing's disease was studied. During several periods (periods lasting up to 84 days) evidence of cortisol hypersecretion with cycles occurring every 6 days was found. Suppression of plasma cortisol through orally administered dexamethasone (up to 32 mg per day) could not be achieved either during periods of cyclic cortisol hypersecretion or during apparent remission with normal cortisol secretion. Marked suppression of plasma ACTH was measured in response to an iv infusion of 50 mg cortisol over a period of 55 min whereas a similar test with 2 mg dexamethasone (iv bolus) did not suppress ACTH secretion. Transsphenoidal exploration of the sella revealed a tumour surrounding the anterior pituitary. Examination of the pituitary showed a few tiny tumour structures embedded in normal tissue which could not be removed, when the tumour was resected selectively under preservation of normal appearing tissue. Post-operatively, clinical and chemical remission (normal response to 1 mg dexamethasone) was observed for about 4 months. Thereafter, cortisol hypersecretion occurred again necessitating bilateral adrenalectomy. Our results are compatible with the assumption that normal hypothalamic-pituitary-adrenal suppressibility with cortisol, but not with dexamethasone, was caused by the loss of feedback receptors for dexamethasone in the presence of cortisol receptors in the cells which secrete ACTH or CRF. The combination of cyclic hypercortisolism with dexamethasone non-suppressible Cushing's syndrome has not been reported before and thus represents a new variant of Cushing's syndrome.


1986 ◽  
Vol 250 (1) ◽  
pp. E87-E93
Author(s):  
W. C. Engeland

Comparisons of resting plasma adrenocorticotropin (ACTH) and corticosterone in the morning and afternoon were made among adult rats bearing regenerated adult adrenal grafts, neonatal (day 1) adrenal grafts, adult adrenal capsule grafts, or intact adrenals. In the morning plasma ACTH and corticosterone were similar in all rats. In the afternoon, plasma ACTH was elevated in rats bearing neonatal adrenal grafts or adult adrenal capsule grafts, but not in rats bearing whole adult adrenal grafts. There was no difference in afternoon plasma corticosterone among rats bearing transplanted adrenals, although afternoon plasma corticosterone was decreased in rats bearing transplants compared with rats with intact adrenals. Thus the increased plasma ACTH after adrenal transplantation cannot be explained entirely by decreases in resting plasma corticosterone. Adrenal responsiveness to ACTH was tested at 5 wk after transplantation in the afternoon by measuring the plasma corticosterone response to submaximal doses of ACTH. The responsiveness was decreased in rats bearing transplants. In addition, responsiveness was inversely related to the age of the grafted adrenal tissue. Adrenals regenerated from adult adrenals were more responsive than adrenals regenerated either from neonatal adrenals or from adult adrenal capsules. The findings suggest that following adrenal transplantation reestablishment of normal pituitary-adrenocortical function does not occur in rats bearing adrenals regenerated from immature adrenal cells. In addition, comparable alterations occur after regeneration of adrenal tissue from neonatal adrenal cells and adult adrenal capsular cells. Elevated plasma ACTH associated with adequate plasma corticosterone in rats bearing adrenals regenerated from immature adrenal cells may result from chronic alteration in responsiveness to steroid feedback.(ABSTRACT TRUNCATED AT 250 WORDS)


1963 ◽  
Vol 109 (461) ◽  
pp. 480-484 ◽  
Author(s):  
V. Marks ◽  
R. G. Bannister

Urinary excretion of adrenal metabolites, especially neutral 17-ketosteroids, is often low in patients with anorexia nervosa (Escamilla, 1949; Bliss and Branch, 1960). This has been taken (Emanuel, 1956; Greenblatt et al., 1951) to provide evidence of adreno-cortical insufficiency secondary to defective pituitary function (Sheldon, 1939; Perloff et al., 1954). According to Perloff et al. (1954) “prolonged starvation may result in functional hypopituitarism, whose differentiation from the syndrome of hypopituitary cachexia due to structural impairment of the anterior pituitary gland is at times extremely difficult, even when the accepted tests for endocrine adequacy are performed”.


2019 ◽  
Vol 85 (10) ◽  
pp. S237
Author(s):  
Stefan Ehrlich ◽  
Viola Borchardt ◽  
Martin Walter ◽  
Maria Seidel

2011 ◽  
Vol 12 (6) ◽  
pp. 455-461 ◽  
Author(s):  
Palmiero Monteleone ◽  
Pasquale Scognamiglio ◽  
Alessio Maria Monteleone ◽  
Daniele Mastromo ◽  
Luca Steardo ◽  
...  

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