Obesity is associated with multiple adverse medical effects. It is a well-known cardiovascular risk factor that leads to an increase in the incidence of diabetes, puts stress on the skeletal system, and is associated with an increase in the risk for certain cancers.  Endometrial cancer is most common in the fifth and sixth decades of life. The risk for endometrial cancer has long been linked to obesity. .

This excess risk is associated with the endocrine and inflammatory effects of adipose tissue.

This is the science behind it:

Adipocytes express aromatase that converts ovarian androgens into estrogens, which induce endometrial proliferation. Sex hormone-binding globulin levels are lower in obese women, and therefore the level of unbound, biologically active hormone is higher. In addition, insulin action is often altered in obese women: The level of insulin-binding globulins is reduced and free insulin levels are elevated. Insulin and insulin-like growth factors (IGF) also exert a proliferative effect on the endometrium, together with other growth factors (eg, epidermal growth factor). Insulin and IGF stimulate endometrial proliferation through pathways that are already hyperactive in women at risk for endometrial cancerhis .

Also, adipose tissue secretes inflammatory factors called adipokines. These factors are partly responsible for the insulin resistance that accompanies obesity and therefore play a role in the augmented endometrial proliferation. Adiponectin, also produced by adipose tissue, has an inhibiting effect on the proliferation pathways. The level of adiponectin is inversely correlated with fat mass. Therefore, numerous pathways (including androgen to estrogen conversion by aromatase; elevated free estrogen, insulin, and IGF levels; increased secretion of inflammatory adipokines; and a lower adiponectin level) can explain the increased risk for endometrial cancer in obese women

Schmandt RE, Iglesias DA, Co NN, Lu KH Am J Obstet Gynecol. 2011;205:518-525