Recent epidemiological and animal studies have suggested that excess intake of phosphate (P-i) is a risk factor for the progression of chronic kidney disease and its cardiovascular complications. However, little is known about the impact of dietary high P-i intake on the development of metabolic disorders such as obesity and type 2 diabetes. In this study, we investigated the effects of dietary P-i on glucose and lipid metabolism in healthy rats. Male 8-wk-old Sprague-Dawley rats were divided into three groups and given experimental diets containing varying amounts of P-i, i.e., 0.2 [low P-i (LP)], 0.6 [control P-i (CP)], and 1.2% [high P-i (HP)]. After 4 wk, the HP group showed lower visceral fat accumulation compared with other groups, accompanied by a low respiratory exchange ratio (V) over dot(CO2)/(V) over dot(O2)) without alteration of locomotive activity. The HP group had lower levels of plasma insulin and nonesterified fatty acids. In addition, the HP group also showed suppressed expression of hepatic lipogenic genes, including sterol regulatory element-binding protein-1c, fatty acid synthase, and acetyl-CoA carboxylase, whereas there was no difference in hepatic fat oxidation among the groups. On the other hand, uncoupling protein (UCP) 1 and peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1 alpha) expression were significantly increased in the brown adipose tissue (BAT) of the HP group. Our data demonstrated that a high-P-i diet can negatively regulate lipid synthesis in the liver and increase mRNA expression related to lipid oxidation and UCP1 in BAT, thereby preventing visceral fat accumulation. Thus, dietary P-i is a novel metabolic regulator.