Won Hee Choi1, Min Young Um2, Jiyun Ahn1, Chang Hwa Jung1, Tae Youl Ha3. 1. Metabolism and Nutrition Research Group, Korea Food Research Institute, Seongnam, Republic of Korea; Division of Food Biotechnology, University of Science and Technology, Daejeon, Republic of Korea. 2. Metabolism and Nutrition Research Group, Korea Food Research Institute, Seongnam, Republic of Korea. 3. Metabolism and Nutrition Research Group, Korea Food Research Institute, Seongnam, Republic of Korea; Division of Food Biotechnology, University of Science and Technology, Daejeon, Republic of Korea. Electronic address: Tyhap@krfi.re.kr.
Abstract
OBJECTIVE: The aim of this study was to evaluate the effects of rice as a carbohydrate source and its molecular mechanisms on insulin resistance induced by a high-fat diet (HFD). METHODS: C57 BL/6 J mice were divided into three groups and were fed a low-fat diet (LFD); a HFD (with 18% fat, 0.5% cholesterol, 51.5% w/w cornstarch and sucrose); or a HFD with rice (HFD-CR, with 18% fat, 0.5% cholesterol and 51.5% w/w rice powder) for 12 wk. In the HFD-CR diet, cooked rice powder was substituted for cornstarch and sucrose in the HFD as a carbohydrate source. RESULTS: HFD-CR-fed mice had significantly lower body weight, blood glucose, insulin and leptin levels and ameliorated glucose responses with decreased homeostasis model assessment-insulin resistance compared with HFD-fed mice. Hepatic mRNA levels of phosphoenolpyruvate carboxykinase and glucose-6-phosphatase were down-regulated in the HFD-CR group. The hypertrophied islet size and the decreased pancreatic mRNA expression of glucose transporter 2 in the HFD group were normalized with cooked rice consumption. Rice promoted glucose uptake by activating AMP-activated protein kinase and downstream glucose transporter 4 in the skeletal muscle. CONCLUSION: Rice consumption as a carbohydrate source might potentiate improvements in glucose uptake via AMP-activated protein kinase activation and glucose transporter 4 expression in the skeletal muscles, thereby improving insulin sensitivity.
OBJECTIVE: The aim of this study was to evaluate the effects of rice as a carbohydrate source and its molecular mechanisms on insulin resistance induced by a high-fat diet (HFD). METHODS: C57 BL/6 J mice were divided into three groups and were fed a low-fat diet (LFD); a HFD (with 18% fat, 0.5% cholesterol, 51.5% w/w cornstarch and sucrose); or a HFD with rice (HFD-CR, with 18% fat, 0.5% cholesterol and 51.5% w/w rice powder) for 12 wk. In the HFD-CR diet, cooked rice powder was substituted for cornstarch and sucrose in the HFD as a carbohydrate source. RESULTS: HFD-CR-fed mice had significantly lower body weight, blood glucose, insulin and leptin levels and ameliorated glucose responses with decreased homeostasis model assessment-insulin resistance compared with HFD-fed mice. Hepatic mRNA levels of phosphoenolpyruvate carboxykinase and glucose-6-phosphatase were down-regulated in the HFD-CR group. The hypertrophied islet size and the decreased pancreatic mRNA expression of glucose transporter 2 in the HFD group were normalized with cooked rice consumption. Rice promoted glucose uptake by activating AMP-activated protein kinase and downstream glucose transporter 4 in the skeletal muscle. CONCLUSION:Rice consumption as a carbohydrate source might potentiate improvements in glucose uptake via AMP-activated protein kinase activation and glucose transporter 4 expression in the skeletal muscles, thereby improving insulin sensitivity.