Hormonal and cellular regulation of Sertoli cell anti-Müllerian hormone production in the postnatal mouse

Anti-Müllerian hormone (AMH) is secreted by immature testicular Sertoli cells. Clinical studies have demonstrated a negative correlation between serum AMH and testosterone in puberty but not in the neonatal period. We investigated AMH regulation using mouse models mimicking physiopathological situat...

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Bibliographic Details
Published in:The Journal of clinical investigation 1997-09, Vol.100 (6), p.1335-1343
Main Authors: Al-Attar, L, Noël, K, Dutertre, M, Belville, C, Forest, M G, Burgoyne, P S, Josso, N, Rey, R
Format: Article
Language:English
Subjects:
Aging
Animals
Animals, Newborn
Anti-Mullerian Hormone
Biochemistry
Biochemistry, Molecular Biology
Blotting, Northern
CHO Cells
Cricetinae
Down-Regulation - drug effects
Enzyme-Linked Immunosorbent Assay
Follicle Stimulating Hormone - pharmacology
Glycoproteins
Gonadotropins, Equine - pharmacology
Growth Inhibitors - biosynthesis
Growth Inhibitors - blood
Growth Inhibitors - genetics
Immunohistochemistry
Life Sciences
Male
Meiosis - physiology
Mice
Mice, Inbred CBA
Mice, Mutant Strains
Molecular biology
Receptors, Androgen - analysis
Receptors, Androgen - genetics
Reproductive Biology
RNA - analysis
Sertoli Cells - metabolism
Sexual reproduction
Testicular Hormones - biosynthesis
Testicular Hormones - blood
Testicular Hormones - genetics
Testis - chemistry
Testosterone - analysis
Testosterone - physiology
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Summary:Anti-Müllerian hormone (AMH) is secreted by immature testicular Sertoli cells. Clinical studies have demonstrated a negative correlation between serum AMH and testosterone in puberty but not in the neonatal period. We investigated AMH regulation using mouse models mimicking physiopathological situations observed in humans. In normal mice, intratesticular, not serum, testosterone repressed AMH synthesis, explaining why AMH is downregulated in early puberty when serum testosterone is still low. In neonatal mice, AMH was not inhibited by intratesticular testosterone, due to the lack of expression of the androgen receptor in Sertoli cells. We had shown previously that androgen-insensitive patients exhibit elevated AMH in coincidence with gonadotropin activation. In immature normal and in androgen-insensitive Tfm mice, follicle stimulating hormone (FSH) administration resulted in elevation of AMH levels, indicating that AMH secretion is stimulated by FSH in the absence of the negative effect of androgens. The role of meiosis on AMH expression was investigated in Tfm and in pubertal XXSxrb mice, in which germ cells degenerate before meiosis. We show that meiotic entry acts in synergy with androgens to inhibit AMH. We conclude that AMH represents a useful marker of androgen and FSH action within the testis, as well as of the onset of meiosis.
ISSN:0021-9738
1558-8238
DOI:10.1172/jci119653