胰岛素抵抗(IR)是多囊卵巢综合征(PCOS)发病的重要病理生理基础,雷帕霉素靶蛋白(mTOR)通路过度激活可导致IR,为PCOS患者多种细胞IR的机制之一。PCOS患者体内高雄激素环境也通过mTOR通路加重细胞IR。高胰岛素血症促进卵巢雄激素的合成,增多的雄激素加重全身细胞IR。卵巢细胞同样存在IR,mTOR通路在其中的作用有待进一步挖掘。 Insulin resistance (IR) is an important pathophysiological basis for the pathogenesis of PCOS. Over-activation of the mTOR pathway leads to IR, which is one of the mechanisms of various cellular IRs in PCOS. The hyperandrogenic environment in PCOS patients also aggravates cellular IR through the mTOR pathway. Hyperinsulinemia promotes ovarian androgen synthesis, and increased androgens increase systemic IR. Ovarian cells also exist IR, mTOR pathway in which the role to be further explored.