A role for estrogens in regulating blood glucose homeostasis is no longer in question. Glycemia is a process finely controlled by the interplay of several tissues: brain, skeletal muscle, liver, adipose tissue and endocrine pancreas. Failure to regulate blood glucose levels leads to the development of type 1 and type 2 diabetes. Type 2 diabetes is the combination of insulin resistance and pancreatic β-cell failure. Evidence both in humans and in animals show that lack of estrogens alters blood glucose homeostasis. Additionally, exogenous estrogens may also affect glycemia. The estrogen receptor alpha, ERα, seems to be the main receptor responsible for most of the effects of estrogens in glycemia. ERβ involvement is still under study, although it is suggested to play a negative role. GPR30/GPER participation in the estrogenic effects is a matter of controversy, mainly due to the different metabolic phenotype of the four GPR30-deficient mice produced. The existence of other receptors for estrogens has been suggested in other systems. However, the role they may be playing in the effect of estrogens in blood glucose levels is still understudied. In this review we present a summary of the complex system responsible for controlling blood glucose homeostasis, the regulation by estrogens and the participation of the different receptors molecularly characterized. However, more research is required to unveil the specific role of each receptor in the modulation of blood glucose homeostasis by the hormone.