Abstract: It has been observed the ovarian dysgenesis exhibited in androgen receptor (ar) knockout female zebrafish, with significant decreased gonadosomatic index (GSI) and expression levels of lhcgr and foxl2, reflecting reduced proportion of mature oocytes. However, the mechanism relating to the androgen receptor in ovarian development is still unknown. The mechanism of ar-deficiency for the ovarian dysgenesis in female zebrafish has been further explored in this study. The significantly reduced levels of vitellogenin (Vtg) production and estrogen receptor expressions have been seen in the liver of ar^–/– females. The ovarian mass, lipid content and carotenoid content decreased significantly, indicates a reduced supply of nutrients such as lipid and carotenoids transferred via Vtg to the ovary in ar^–/– females. Besides, the correlation between the significantly downregulated transcriptional expression levels of several key genes related with the ovarian development and the stagnation of ovarian development has been observed in the ar^–/– females. Our results demonstrate that the ar-deficiency downregulates the estrogen receptors in the liver, impairs the Vtg transportation and yolk formation in the ovaries, and ultimately disrupts ovarian development. This study shed light on the connection between the androgen signaling and hepatic Vtg production in vivo.