加体外培养的正常黄体颗粒细胞ObR mRNA的表达，且当LEP浓度在100 ng/mL时，ObR mRNA的表达达到高峰[14]，说明具有PCOS的肥胖女性，其血清LEP浓度增高，可促进黄体颗粒细胞ObR表达增高，进而增加对LEP的敏感性，这可能与PCOS肥胖女性排卵停止有关。因此，笔者认为实验中PCOS大鼠卵巢ObR表达异常增强，将激活更多LEP发挥作用，增强对卵巢功能的抑制，导致PCOS不排卵，以至于生育力下降。
ObR及其mRNA在卵巢的定位表达表明LEP通过ObR对卵巢功能有直接的影响。PCOS大鼠卵巢中ObR表达增强，导致LEP对卵巢功能的抑制增强，直接参与PCOS发病机制中卵巢功能的异常调节，至于是否存在受体后信号传导的异常尚需进一步研究得以证实。
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