Early studies demonstrated that whole‐body androgen receptor (AR)–knockout mice with hypogonadism exhibit insulin resistance. However, details about the mechanisms underlying how androgen/AR signaling regulates insulin sensitivity in individual organs remain unclear. We therefore generated hepatic AR‐knockout (H‐AR−/y) mice and found that male H‐AR−/y mice, but not female H‐AR−/− mice, fed a high‐fat diet developed hepatic steatosis and insulin resistance, and aging male H‐AR−/y mice fed chow exhibited moderate hepatic steatosis. We hypothesized that increased hepatic steatosis in obese male H‐AR−/y mice resulted from decreased fatty acid β‐oxidation, increased de novo lipid synthesis arising from decreased PPARα, increased sterol regulatory element binding protein 1c, and associated changes in target gene expression. Reduced insulin sensitivity in fat‐fed H‐AR−/y mice was associated with decreased phosphoinositide‐3 kinase activity and increased phosphenolpyruvate carboxykinase expression and correlated with increased protein‐tyrosine phosphatase 1B expression. Conclusion: Together, our results suggest that hepatic AR may play a vital role in preventing the development of insulin resistance and hepatic steatosis. AR agonists that specifically target hepatic AR might be developed to provide a better strategy for treatment of metabolic syndrome in men. (HEPATOLOGY 2008.)