In this study we provide direct evidence that using the ArKO mouse model, which has no aromatase and hence essentially zero levels of estrogens, allowed us to investigate the effects of exogenous estrogens on the management of glucose metabolism without the interference of endogenous estrogen production and determined that estrogen deficiency leads to hepatic glucose intolerance which precedes the development of male-specific hepatic steatosis. The gene discussed is CYP19A1; the disease is fatty liver disease.