Abstract
Age-related decreases in Leydig cell testosterone production are not restored by exposure to LH in vitro
Chen,Haolin; Hardy,Matthew P.; Zirkin,Barry R.
Endocrinology 143(5): 1637-1642
Publication date: 2002
Aging in Brown Norway rats is associated with reduced Leydigcell T production. To address the mechanism by which aging Leydigcells become steroidogenically hypofunctional, Leydig cellsfrom young and old rat testes were isolated and cultured long-termwith LH. Leydig cells isolated from young rats that had receivedLH-suppressive T implants served as positive controls. The abilityof young control Leydig cells to produce T at high levels wassustained over a 3-d culture period. T production by cells fromyoung LH-suppressed rats increased over this period, almostto control levels. In contrast, culture of the steroidogenicallyhypofunctional old Leydig cells with LH failed to increase theirT production, suggesting that LH stimulation, by itself, isunable to reverse the steroidogenic deficits of old Leydig cells.Reduced numbers of LH binding sites characterized Leydig cellsfrom old rats and LH-suppressed young rats. However, whereasLeydig cells from young LH-suppressed rats produced cAMP atthe high levels of young control cells, the old cells producedfar less cAMP, suggesting that old Leydig cells have defectsin the LH-cAMP signaling cascade. When stimulated with forskolin,old cells produced the same amount of cAMP as young controland young LH-suppressed cells, suggesting that adenylate cyclaseis maintained in the old cells. Taken together, these resultssuggest that inefficient signal transduction may explain thereduced steroidogenesis that characterizes old Leydig cells.
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