Abstract
Gonadotropin secretion is inhibited by the endogenous opioids and stimulated by their antagonist naloxone. LH secretion is stimulated by α-MSH, a tridecapeptide derived from the post-translational processing of POMC. The possibility that α-MSH interacts with the opioids, as suggested by the experimental evidence, was investigated in 7 normal males aged 24–29 through the performance of seven tests: naloxone (0.8 mg iv bolus, followed by infusion of 1.6 mg/h for 120′); α-MSH (2.5 mg iv bolus); naloxone+α-MSH (2.5 mg i.v. 15′ after commencement of the naloxone infusion); naloxone+GnRH (100 µg iv 15′ after commencement of the naloxone infusion); α-MSH+GnRH (respectively 2.5 mg and 100 µg at time 0), GnRH alone (100 µg at time 0), placebo (150 nmol/l NaCl solution). The LH AUCs during both naloxone (30.3±2.7 mlU/ml.min−1) and α-MSH test (32.9±4.6 mlU/ml.min−1) were significantly greater (p < 0.005) than that observed during placebo (16.9±3.6 mlU/ml.min−1). The LH AUC during α-MSH+naloxone (37.6±2.6 mlU/ml.min−1) was not significantly different from that recorded during their separate administration. GnRH injected alone, during the naloxone infusion and with α-MSH produced similar increases in LH, that were significantly higher than that observed during the other tests (AUCs: GnRH 89.4±10.6, GnRH+naloxone 100.5±9.1, GnRH+α-MSH 94.6±7.9 mlU/ml.min1, p<0.001). Significant increase in FSH (p<0.001) was only observed during GnRH, GnRH+naloxone and GnRH+aMSH tests (AUCs: placebo 13.3±1.7; naloxone 14.7±2.5; α-MSH 15.5±2.3; α-MSH+naloxone 16.9+1.9; GnRH 19.1 ±1.1; GnRH+α-MSH 20.7±1.3; GnRH+naloxone 21.2±1.8 mlU/ml.min−1). These results are in line with the possibility of an interaction between α-MSH and the opioids in the regulation of gonadotropin secretion, perhaps with opposing effects on a final common pathway.
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Limone, P., Calvelli, P., Altare, F. et al. Evidence for an interaction between α-MSH and opioids in the regulation of gonadotropin secretion in man. J Endocrinol Invest 20, 207–210 (1997). https://doi.org/10.1007/BF03346904
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DOI: https://doi.org/10.1007/BF03346904