The Role of Endogenous Opiates in the Mechanism of Inhibited Luteinizing Hormone (LH) Secretion in Women with Anorexia Nervosa: The Effect of Naloxone on LH, Follicle-Stimulating Hormone, Prolactin, and β-Endorphin Secretion*

Abstract

The aim of this study was to evaluate the role of endogenous opiates in the mechanism of decreased LH secretion in women with anorexia nervosa. For this purpose the effect of opiate receptor blockade with naloxone on LH, FSH, PRL, and beta-endorphins secretion was studied in 24 women with anorexia nervosa and 7 normal women. Serum LH, FSH, PRL, beta-endorphin-like substance, ACTH, and cortisol concentrations were measured before and after opiate receptor blockade after a single iv dose of 0.2 mg/kg naloxone or saline. Mean serum LH and FSH concentrations increased significantly after naloxone in the normal women. Eleven patients had a significant increase in serum LH concentrations in response to naloxone and 13 did not respond to naloxone with an increase in LH concentration. In the first group the basal LH values were higher than those in the second group. In the majority of patients in the first group amenorrhea preceded the wt loss, whereas in most patients in the second group amenorrhea appeared during the phase of wt loss. Naloxone did not alter pulsatile LH secretion in 6 women. No effect of naloxone on serum FSH and PRL concentrations was found. A significant increase in beta-endorphin-like substance levels after naloxone administration occurred in patients with anorexia nervosa. However, serum ACTH and cortisol concentrations were not altered in response to naloxone. In conclusion, the increase in LH release after opiate receptor blockade by naloxone suggests that endogenous opiates may play a role in the mechanism of inhibited LH secretion at least, in the majority of those women with anorexia nervosa in whom amenorrhea preceded wt loss. The results also point to a different mechanism of ACTH and beta-endorphin secretion in patients with anorexia nervosa.

Naltrexone potentiates 4-aminopyridine seizures in the rat

“…However, very little is known about the effects of bolus administration (Kosten et al, 1986). No changes in receptor density were found 30 min after the injection of 10mg/kg naltrexone (Tempel et al, 1984), and the awaited elevation of beta-endorphin levels in blood or in brain structures could not be proven (H611t et al, 1978;Wtister et al, 1980;Baranowska et al, 1984;Kosten et al, 1986). One can only hypothesize, that due to receptor blockade, the amount of enkephalins and beta-endorphins (which are known to interact with mu receptors-- Klosterlitz, 1985) increases in the extracellular space, but their regulatory function can not be fulfilled.…”

The role of opiate, dopaminergic, and adrenergic systems in the hypothalamo-pituitary dysfunction in obesity

“…Serum GH, LH, PRL and cortisol concentrations were measured using RIA methods previously described in detail (Stupnicki 1979;Midgley 1966;McNeilly 1973;Jeske 1979;Baranowska et al 1984). Plasma ß-endor¬ phin was measured by radioimmunoassay, after initial extraction with silic acid (Merck, Germany) according to 120 TIME (min.…”

Amenorrhea in anorexia nervosa neuroendocrine control of hypothalamic dysfunction

“…Endogenous opioids are known to modulate GnRH-mediated gonadotropin release (Yen, Quigley, Reid, Ropert, & Cetel, 1985) but attempts at measuring the LH response to opiate receptor blockade in women with anorexia nervosa have produced conflicting results. Baranowska et al (1984) found a significant LH response to naloxone in 11 of 24 women with anorexia nervosa. Of interest is that in those who responded to naloxone, amenorrhea preceded weight loss whereas it followed weight loss in those who did not respond to naloxone.…”