Scanelli G

Testosterone and calcitonin plasma levels in hypogonadal osteoporotic young men

The aim of this study was to ascertain whether there was an interrelationship between male osteoporosis, calcitonin and androgens. Ten young hypogonadal osteoporotic men were studied: testosterone and calcitonin plasma levels were measured before and after therapy with testosterone enanthate (200 mg im every three weeks for four months). In these patients testosterone and calcitonin plasma levels were significantly lower than controls, before therapy (p < 0.001 and p < 0.01 respectively). Testosterone treatment significantly increased (p < 0.05) serum calcitonin. The conclusion was that androgen deficiency may cause osteoporosis also by decreasing calcitonin secretion.

Gonadal steroids and opioid control of gonadotropin secretion in man

The aim of this study was to ascertain whether there was an interrelationship between gonadal steroids and endogenous opioid peptides. The effects of naloxone (20 mg, intravenously) and of a met-enkephalin analog (DAMME) (250 micrograms, intravenously) on gonadotropin secretion in three castrated men (18 to 23 years of age) and in five age-matched normal men were studied. Normal subjects were studied before and after treatment with a specific nonsteroidal estrogen receptor antagonist, clomiphene. Naloxone caused a significant increase in luteinizing hormone (LH) (P less than 0.05); in these subjects, clomiphene treatment significantly increased LH and follicle-stimulating hormone plasma levels but totally suppressed the naloxone-induced rise in LH. In castrated men, naloxone failed to increase plasma LH levels. However, DAMME significantly reduced plasma LH levels in normal, in castrated, and in clomiphene-treated normal subjects. The results demonstrate that in castrated subjects who lack gonadal steroids and in normal subjects with blocked estrogen receptors there is a reduced opioid inhibitory tone on gonadotropin secretion. The effect of DAMME on gonadotropin secretion, however, is not influenced by the gonadal steroid environment.

NALOXONE REDUCES THE FENFLURAMINE‐INDUCED PROLACTIN RELEASE IN MAN

In order to ascertain whether there is a relation between opioids and the serotoninergic system in prolactin (PRL) secretion increase, we investigated in seven healthy men (21 to 26 years of age) the effect of naloxone, a specific opioid antagonist, on PRL secretion induced by fenfluramine, a drug that stimulates serotonin release and inhibits its re‐uptake. We observed that subjects receiving fenfluramine (60 mg orally) had a significantly (P < 0·001) higher increase in PRL plasma levels than the controls receiving placebo. In all subjects naloxone infusion at a dose of 15 mg caused a significant reduction (P < 0·0005) in the PRL response to fenfluramine. Higher doses of naloxone (30 mg) do not further inhibit the PRL secretion induced by fenfluramine. These results suggest that naloxone may interact with opiate receptors on serotonin neurons thereby reducing the synthesis and release of serotonin. It seems that in man, therefore, there is an interplay between opiates and the serotoninergic system in the facilitatory influence on PRL release.

Evidence of sperm nuclear chromatin heterogeneity in ex-cryptorchid subjects

Summary:  Ex‐ctyptorchid subjects are frequently affected by infertility, even if the usually determined seminal parameters are still within the normal range. We evaluated in this study, in 14 ex‐unilateral cryptorchid adult males (22–28 years), with normal sperm concentration, morphology and viability, the resistance of sperm nuclear chromatin to de‐naturation, using the fluorochrome acridine orange, which fluorescences green when bound to native DNA (double stranded) and red when bound to denaturated DNA (single stranded).

Serotonin but not dopamine is involved in the naloxone-induced luteinizing hormone release in man

Endogenous opioid peptides exert a tonic inhibition on gonadotropin secretion at the hypothalamic level, but the mechanisms by which they act are still unknown. Previous experimental studies suggest that the endogenous opioid peptides change dopaminergic and serotoninergic tones at the hypothalamic level. We have investigated whether the stimulatory effect of naloxone on luteinizing hormone (LH) secretion is due to its influence on these neurotransmitters. Two experimental models were studied, and two sets of effects on LH secretion induced by intravenous naloxone infusion (20 mg over 2 hours) in 14 normal men 20 to 25 years of age were evaluated: the effect of oral sulpiride (150 mg), a potent dopaminergic antagonist, and the effect of oral fenfluramine (60 mg), a drug that stimulates the serotoninergic receptors by releasing serotonin and inhibiting its reuptake. The study demonstrated that naloxone infusion significantly stimulated the LH secretion throughout the period of observation (P less than 0.01 versus saline). The pretreatment with sulpiride did not change the LH response to naloxone. After fenfluramine pretreatment, naloxone failed to induce any rise in LH secretion. Follicle-stimulating hormone did not show any important variation in either test. The data suggest that in man the stimulatory ability of the opiate receptor antagonist naloxone to elicit a rise in LH plasma levels may involve the serotoninergic, but not the dopaminergic, hypothalamic system. This hypothesis, however, does not exclude the involvement of other hypothalamic neurotransmitters.

The influence of gonadal steroids on the dopamine inhibitory effect on gonadotropin release in men

The aim of this study was to ascertain whether an interrelationship exists between gonadal steroids and the inhibition of gonadotropin secretion by dopamine. The effect of dopamine infusion (4 micrograms/kg/minute intravenously) on gonadotropin plasma levels in four castrated men (18 to 23 years of age) and in four age-matched normal men was studied. Normal subjects were studied before and after treatment with a specific nonsteroidal estrogen receptor antagonist, CC. LH plasma levels in normal subjects receiving CC had a maximum decrease percentage and a net decrease significantly greater (P less than 0.005 and P less than 0.012, respectively) than those before CC treatment. In castrated subjects the maximum decrease percentage was significantly greater (P less than 0.005) than in control subjects, but it did not show any difference from that of normal subjects receiving CC. In none of the group were significant changes in FSH concentration observed. The findings suggest that whenever there is a gonadal steroid deficiency, dopamine infusion causes an increased sensitivity to LH inhibition. This may be due to a lower endogenous dopaminergic influence on LH secretion.