IT HAS BEEN assumed for the last 50 yr that testicular descent is under hormonal control. The exact mechanism has remained unknown, although the general belief in recent years has been that descent is mediated by androgens. Postnatal rodents have provided a convenient model, since descent is incomplete at birth and can be influenced by both exogenous androgens or antiandrogens. Moreover, fetal mice exposed to estrogens have undescended testes, and the inhibitory effect of estrogens can be prevented by simultaneous injection of human CG. These studies have been interpreted as demonstrating inhibition or stimulation of androgen secretion, with consequent effects on testicular descent. The role of androgens has been questioned, however, because antiandrogens, such as cyproterone acetate, fail to block descent in the fetus. Recent studies of children and mice wiith complete testicular feminization associated with androgen resistance also fail to show an effect of androgens in the transabdominal phase of descent. Based on these studies, a biphasic model for the hormonal control of testicular descent has been proposed, with androgens stimulating only the second or transinguinal phase. The first phase could be controlled by Mullerian Inhibiting Substance (MIS), but this thesis remains unproven.
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Hutson et al. (1986) studied this question.