Sun Hee Hong¹, Minji Woo¹, Jeong Sook Noh², Yeong Ok Song^1,

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.

brown rice, diabetes mellitus, ginseng, insulin, lipid metabolism