The current studies indicate that Leydig cells from old (24-27-Mo) rats secreted significantly less cholesterol in
response to stimulators, hCG, forskolin, or Bt2cAMP as compared to cells from young mature (5-Mo) animals. This deficiency
was reversed by incubation of cells with free diffusible hydroxycholesterols, indicating that age-related decline in
testosterone secretion primarily results from the reduced availability of substrate cholesterol. Aging also significantly diminished
the Leydig cell mRNA levels of StAR/StarD1, StarD2 and StarD4 both under basal conditions in response to
hCG stimulation. Likewise, aging decreased the mRNA levels of PBR/TSPO. These changes correlated well with the reduced
accumulation of cholesterol in Leydig cell mitochondria from old animals. Our results suggest that aging caused
impaired expression of key cholesterol transport proteins, StAR/StarD1, StarD4 and PBR/TSPO that resulted in inefficient
delivery of cholesterol to and within the mitochondria, and subsequently reduced conversion of cholesterol to
pregnenolone and decreased testosterone production.
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