作者: Stephen M. Eacker , Robert E. Braun
DOI: 10.1007/978-1-59745-453-7_24
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摘要: Testosterone (T) is a critical regulator of sexual differentiation and spermatogenesis in mammals. The effects T are mediated by the androgen receptor (AR), nuclear hormone transcription factor. AR expressed many cell types throughout organism including T-secreting Leydig cells (LCs). Although, its expression pattern fetal generation LC unclear, maturation adult LCs. Expression required for normal development as assessed morphology, steroid output, markers maturation. LCs human bearing mutations Ar, lack crystals Reinke secrete large amount estrogen to high levels T. In contrast, mice that have congenital mutation Ar produce less than their wild-type littermates small, lipidladen with reduced volume smooth endoplasmic reticulum. Marker gene analysis show lacking fail express number genes associated Rats mutant similar defects morphology steroidogenic activity. Within context testis, functions an ultrashort feedback loop repress expression. Mutations predispose all mammals testicular neoplasia, tumors. mechanism tumor induction mutants remains unclear. Together, studies discussed this chapter plays role function development.