Gonadal hormones inhibin A and inhibin B (a/bA or a/bB heterodimers) are classically known for their abilities to constrain follicle stimulating hormone (FSH) production from pituitary gonadotroph cells. It is largely accepted that inhibins downregulate FSHB transcription by disabling receptor activation by related activins (bA/B/bA/B dimers). Beyond FSH regulation, roles for inhibins in female and male fertility have been poorly understood owing to a lack of appropriate physiological models. Here, armed with new mouse models of dysregulated inhibins we have uncovered novel roles for inhibins in gonadal function and fertility. Our, and supporting works by our collaboration at McGill University (Montreal), have shown that maintenance of inhibin physiological activity is important not only for FSH regulation, but also for embryo and foetal survival during pregnancy in female mice. Additionally, together we have uncovered evidence to support that partial inactivation of inhibins actually enhances fertility in female mice. More recently we have discovered that persistent inhibin inactivity in female mice is associated with the development of polycystic ovaries. Serendipitously, using these inhibin inactivated mouse models we have also identified roles for inhibins in the regulation of adiposity in females. Significantly, as these phenotypes pertain only to female mice, we are unveiling new sex-specific activities for the inhibins. Ultimately these findings signify inhibins as not only gatekeepers of female reproductive health, but also metabolic health.