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Objectives: The prevalence of nonalcoholic fatty liver disease (NAFLD) has increased alongside obesity and is much higher in postmenopausal women than in men and premenopausal women. In addition, the adipose tissue growth and expansion that cause obesity are known to be related to angiogenesis. We, therefore, investigated whether 17β-estradiol can regulate obesity and NAFLD in high-fat diet (HFD)–fed obese ovariectomized (OVX) C57BL/6J mice, a mouse model of postmenopausal women, and explored the involvement of angiogenesis and vascular endothelial growth factor A (VEGF-A) in this process. Methods: The effects of 17β-estradiol on NAFLD and angiogenesis were examined using histological analysis, immunohistochemistry, and quantitative real-time polymerase chain reaction. Results: When HFD–fed obese OVX mice were treated with 17β-estradiol for 8 weeks, they exhibited decreases in body weight and total adipose tissue weight. 17β-estradiol not only reduced serum levels of alanine aminotransferase but also inhibited hepatic steatosis, inflammation, and fibrosis. Furthermore, blood vessel density and VEGF-A mRNA expression were decreased by 17β-estradiol in the visceral adipose tissue of obese OVX mice. Conclusion: These results suggest that 17β-estradiol regulates obesity and NAFLD in part by reducing angiogenesis and VEGF-A in obese OVX female mice.