Effects of Ginseng-Added Brown Rice Cookie on the Regulation of Hepatic Glucose Metabolism Mediated through the Insulin Signaling Pathway in &lt;i&gt;db/db&lt;/i&gt; Obese Mice

Sun Hee Hong,Minji Woo,Yeong Ok Song,Jeong Sook Noh

doi:10.12691/jfnr-6-4-6

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 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 P P P 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.

Highlights

Type 2 diabetes mellitus (T2DM) is characterized by insulin resistance, impaired glucose tolerance, and dyslipidemia [1]
The amelioration of insulin resistance mediated through regulation of the insulin signaling pathway is considered a practical T2DM treatment [29]
The plasma insulin level and area under the curve (AUC) in the ginseng-added brown rice cookie (GBRC) group were decreased, indicating that the insulin resistance was lowered. These results might be due to an elevation of insulin sensitivity mediated through activation of the insulin signaling pathway, especially in the liver, given that hepatic p-insulin receptor substrate (IRS) and p-Akt were significantly upregulated in the GBRC group

Summary

Introduction

Type 2 diabetes mellitus (T2DM) is characterized by insulin resistance, impaired glucose tolerance, and dyslipidemia [1]. Insulin plays a critical role in controlling the plasma glucose level during the fed state by stimulating glucose uptake in the liver and muscles. The insulin resistance observed in obesity-related T2DM is caused by a decrease in insulin receptor activity. Insulin sensitivity is dependent on the insulin signaling pathway, known as the insulin receptor substrate (IRS)-phosphoinositide 3-kinase (PI3K)-Akt pathway, the activation of which stimulates glucose uptake for energy production and glycogen synthesis. 5′ adenosine monophosphate-activated protein kinase (AMPK), a key enzyme for energy production, activates the IRS-. PI3K-Akt pathway but inhibits gluconeogenesis [2], the latter of which is the opposite of glycolysis and an important regulatory process for maintaining plasma glucose levels during fasting or starvation. Pyruvate carboxykinase (PCK) and glucose-6-phosphatase (G6Pase) are the main enzymes involved in gluconeogenesis [3]

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