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. CONCLUSIONS 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.