In the present study, the effects of ginseng-added brown rice cookie (GBRC) on the regulation of hepatic glucose and lipid metabolism mediated through the insulin signaling pathway were examined in db/db mice. Isocaloric diets, prepared by adding the individual ingredients of rice cookie (RC) or GBRC to AIN-93G diet (10%, w/w), were fed to the animals for 10 weeks (n = 7 per group). The plasma insulin level and oral glucose tolerance test-derived area under the curve were lower in the GBRC group than in the RC group (P < 0.05). In the GBRC group, the insulin signaling pathway was significantly elevated through phospho-insulin receptor substrate-1 and phospho-Akt upregulation (P < 0.05), indicating that glucose utilization was increased. Subsequently, hepatic triacylglycerol synthesis was inhibited via the downregulation of fatty acid synthase, regulated by sterol regulatory element binding protein-1. In addition, fatty acid oxidation was increased. Protein expression levels of the lipolytic enzymes carnitine palmitoyltransferase I and acetyl-CoA oxidase 1, regulated by peroxisome proliferator-activated receptor-alpha, were increased (P < 0.05). Consequently, gluconeogenesis was suppressed via the downregulation of gluconeogenic enzymes, such as pyruvate carboxykinase and glucose-6-phosphatase, regulated by phospho-5′ adenosine monophosphate-activated protein kinase (P < 0.05). Protein expression levels of the nuclear factor kappa B-regulated cyclooxygenase-2 and inducible nitric oxide synthase were inhibited, thereby diminishing reactive oxygen species and peroxynitrite generation (P < 0.05). In conclusion, GBRC revealed antidiabetic effects by promoting hepatic glucose utilization mediated through the insulin signaling pathway, which enhanced lipid oxidation rather than triacylglycerol synthesis.