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Journal of Endocrinology (1996) 151, 301-307       DOI: 10.1677/joe.0.1510301
© 1996 Society for Endocrinology
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The steroidogenic effects of β-endorphin and joining peptide: a potential role in the modulation of adrenal androgen production

D Clarke, U Fearon, S K Cunningham and T J McKenna

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 ({Delta}4) and dehydroepiandrosterone (DHEA) production (P<0·05); β-End stimulated only {Delta}4 and DHEA production. β-End brought about significant increases in the {Delta}4 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 {Delta}4 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 {Delta}4 and DHEA levels. This may explain the occurrence of increasing androgen levels at adrenarche.

Journal of Endocrinology (1996) 151, 301–307




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