Growth Hormone and Prolactin Secretion After Growth Hormone‐releasing Hormone Administration, in Anorexia Nervosa Patients, Normal Controls and Tamoxifen‐pretreated Volunteers

Abstract

Anorexia nervosa is associated with several abnormalities in GH secretion elicited by different stimuli. To investigate the precise mechanism of this alteration, GHRH was administered to 14 women: a group of eight anorexia nervosa patients in the acute phase of their illness and a control group of six age-matched volunteers. As patients with anorexia nervosa have chronic low oestrogen values, the volunteer women of the control group underwent a second GHRH test after pretreatment with the oestrogen receptor blocker tamoxifen. GHRH 1-29 (1 microgram/kg i.v.) induced a GH peak (mean +/- SEM) of 28.2 +/- 5.1 ng/ml (GH ng/ml x 2 = mU/l) at 30 min in the anorectic patients. This value was no different from the GHRH-stimulated GH peak in the control women (28.1 +/- 10.0 ng/ml). Tamoxifen pretreated women had a GH peak after GHRH of 35.6 +/- 9.7 ng/ml, not significant versus control test. Compared with the control group, oestrogen levels were significantly lower in anorectic patients and higher in tamoxifen-treated women. GHRH administration induced a small PRL peak at 15 min that was similar in the three groups tested. After this 15 min peak, PRL in both anorexic and tamoxifen-treated women returned toward basal values steadily. However, in untreated control women a second PRL peak was evident at 60 min. In conclusion, GHRH-induced GH secretion in anorexia nervosa patients was similar to that in control subjects and in controls under oestrogen receptor blockade.

Low circulating IGF‐I levels in hyperthyroidism are associated with decreased GH response to GH‐releasing hormone

“…Several pieces of evidence suggest that, acutely, pblockers may increase GH by an inhibition of somatostatin release. In man, @-blockers potentiate the G H response to a maximal GHRH dose (Chihara et al, 1985;Mauras et al, 1987;Martha et al, 1988) and reinstate it when inhibited by a previous GHRH bolus (Arosio et al, 1990). In the rat, pblockers inhibit hypothalamic somatostatin release in vitro (Richardson & Twente, 1990).…”

“…The mechanisms underlying the altered GH secretion in hyperthyroidism are not fully elucidated. Thyroid hormones probably do not exert their effects directly at the pituitary level, since they do not act on human G H gene transcription (Cattini et al, 1986;Brent et al, 1988).…”

Chronic orchidectomy does not influence the sensitivity of the pituitary somatotropes to varying doses of GHRH administered intravenously to the adult male rhesus monkey

“…In a comparable study in normal men, short-term gonadal blockade by a GnRH agonist did not produce significant changes in the responsiveness of pituitary somatotropes to exogenous GHRH (Lima et al, 1989). Likewise, neither short-term hypo-estrogenism in normal women pretreated with tamoxifen (Lima et al, 1989;Casanueva et al, 1987) nor chronic hypo-estrogenism as in anorexia nervosa patients (Casanueva et al, 1987) altered the pituitary response to GHRH. Taken together, these investigations suggest that neither short-term gonadal blockade nor long-term gonadal steroid deprivation affects the responsiveness of the pituitary somatotropes to exogenous GHRH challenge in primates.…”

“…Thus, the mean GH responses of women to GHRH in high estradiol (E 2 ) low progesterone (P) follicular phase of their cycles are not significantly different from those observed in low E 2 high P midluteal phase (Smals et al, 1986;Lima et al, 1989). Furthermore, the GH response to GHRH in women is not affected by short-term estrogen blockade with either tamoxifen, an estrogen receptor antagonist (Casanueva et al, 1987) or with GnRH agonist (Lima et al, 1989) or long-term hypoestrogenism as seen in anorexia nervosa patients (Casanueva et al, 1987).…”

Clonidine Plus GHRH Administration for Diagnosing Growth Hormone Deficiency in Children

“…At this point and although it is not the objective of this study, low plasma IGF-I values do not necessarily reflect GHdeficient secretion. As we recently published, the hepatic expression of IGF-I is strongly conditionated by the intracellular metabolism of glucose [33], therefore poor nutritional conditions may lead to low plasma levels of this factor despite of normal or increased GH secretion, as it happens in Anorexia Nervosa patients [34]. It can occur too in children with strong spasticity due to brain injuries.…”