Many obese adults and adolescents undergo repeated cycles of dietinduced weight loss and gain, a phenomenon known as weight cycling (WC). Epidemiological studies suggest an implication of WC in increased cardiovascular morbidity/mortality. The aim of our study was to establish a rat model of WC to further evaluate its consequences on metabolic and cardiovascular diseases. Experiments were performed in male Sprague Dawley rats, initially fed with normal chow (NC 4.5% fat) for 24 days (d). Time control group I received a fixed amount of 21 g/d. Group II received the same total amount given as cycles of 3 d at -33% (14 g/d) and 3 d at +33% (28 g/d) for a total of 4 cycles. Thereafter, following a 4-d stabilization period at 21 g/d of NC, animals were switched for 14 additional days to 20 g/d of a high fat diet (23.6% fat), an amount isocaloric to 28 g of NC. At the end, a glucose tolerance test (GTT) was performed with determination of plasma glucose and insulin. Visceral fat (retroperitoneal and epididymal) was weighed and total body composition was assessed by the Soxhlet method. Despite similar body weight gain (165.8 ± 3.8 vs. 173.3 ± 2.7 g) in both groups, total body fat and visceral fat were significantly increased in cycling rats (55.6 ± 2.2 vs. 48.6 ± 1.3 g; 16.9 ± 0.8 vs. 13.9 ± 0.5 g). Cycling rats also showed a higher 30-min insulinemic response during the GTT (insulin change from baseline 6.1 ± 1.0 vs. 4.3 ± 0.9 ng/mL). Our data suggest that WC, independently of excess food intake and weight gain, may predispose to the development of cardiovascular diseases by promoting total fat and visceral fat accumulation, as well as insulin resistance.