LEP and breast carcinoma: While the molecular mechanisms underlying the impact of overall and central obesity on poorer breast cancer outcomes are not well understood, it has been hypothesized that the biological effects of the adipokines, adiponectin (ADIPOQ) and leptin (LEP), which are secreted by adipocytes (8–13), and their respective receptors (adiponectin receptors 1 and 2 [ADIPOR1, ADIPOR2] and leptin receptor [LEPR], respectively) might play a role.