Two human mutations have also been reported supporting the contention that fetal testicular steroidogenesis must begin independent of any pituitary LH. A mutation in the LH receptor produces pseudohermaphroditism, with testes and normal wolffian duct derivatives, but few germ cells. This phenotype is consistent with the contention that the testosterone necessary for wolffian duct stabilization is produced independently of LH/hCG action . Another mutation in the LH(3 subunit gene in the human had consequences similar to those produced by the a-subunit gene-deficient mice . The affected male developed with normal male external genitalia and wolffian duct derivatives . However, in this case hCG could have provided a gonadotropic stimulus for the fetal testes. buy asthma inhalers
FrcJm all the above evidence, we can conclude that LH from .the fetal pituitary need not be the initiating factor for testicular steroidogenesis because a nongonadotropic endocrine or paracrine factor might carry out this function. This is supported by our findings in vitro on high basal and hCG-stimulated testosterone production by fetal testes using two different incubation techniques. The significant increase in the basal testosterone production by the fetal testes between E16.5 and E19.5, i.e., before the appearance of significant LH levels in the circulation, points to the presence of such a stimulatory factor. However, when this factor is washed out or diluted during dispersion of the testicular cells, the effect disappears, and the basal testosterone production of fetal Leydig cells remains low. The identity of this activity remains elusive.