The steroidogenic effects of β-endorphin and joining peptide: a potential role in the modulation of adrenal androgen production

Abstract

Abstract This study examines the androgen-stimulating properties of pro-opiomelanocortin-derived peptides, ACTH, β-endorphin (β-End) and joining peptide (JP). Ten different cell suspensions were prepared from ten human adrenal glands. ACTH and JP stimulated cortisol, androstenedione (Δ4) and dehydroepiandrosterone (DHEA) production (P<0·05); β-End stimulated only Δ4 and DHEA production. β-End brought about significant increases in the Δ4 or DHEA to cortisol ratios. The addition of β-End (10−10 m) suppressed ACTH-stimulated cortisol production from 7573 ± 2960 to 5994 ± 2654 pmol/106 cells (means ± s.e.m.; P<0·05). The addition of β-End did not affect ACTH-stimulated Δ4 production (210 ± 88 and 236 ± 105 pmol/106 cells). JP (10−10 m) inhibited ACTH-stimulated cortisol production so that the mean values fell to 5186 ± 2588 and also inhibited DHEA production, from 240 ± 48 to 180 ± 33 pmol/106 cells. These results suggest that the relative production of androgen to cortisol is greater in response to β-End and JP than in response to ACTH. If blood levels of these peptides rise to herald adrenarche as reported for β-End, suppression of cortisol production may result in an increase in ACTH to correct cortisol levels resulting in an increase in Δ4 and DHEA levels. This may explain the occurrence of increasing androgen levels at adrenarche. Journal of Endocrinology (1996) 151, 301–307