@article{jfnr2018646,
author={{Hong, Sun Hee and Woo, Minji and Noh, Jeong Sook and Song, Yeong Ok},
title={Effects of Ginseng-Added Brown Rice Cookie on the Regulation of Hepatic Glucose Metabolism Mediated through the Insulin Signaling Pathway in <i>db/db</i> Obese Mice},
journal={Journal of Food and Nutrition Research},
volume={6},
number={4},
pages={242--249},
year={2018},
url={http://pubs.sciepub.com/jfnr/6/4/6},
issn={2333-1240},
abstract={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 <i>db/db </i>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 (<i>P</i> &lt; 0.05). In the GBRC group, the insulin signaling pathway was significantly elevated through phospho-insulin receptor substrate-1 and phospho-Akt upregulation (<i>P</i> &lt; 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 (<i>P</i> &lt; 0.05). Consequently, gluconeogenesis was suppressed via the downregulation of gluconeogenic enzymes, such as pyruvate carboxykinase and glucose-6-phosphatase, regulated by phospho-5กไ adenosine monophosphate-activated protein kinase (<i>P</i> &lt; 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 (<i>P</i> &lt; 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.},
doi={10.12691/jfnr-6-4-6}
publisher={Science and Education Publishing}
}
