The literature data relate about alloxan diabetic model and its effect on adult rats. However, the Diabetes Mellitus appears when the organism is still rapid development (humans from 9 – 13 years old). Thus, this research studied the development of diabetic disease (period of 60 days) when the drug was injected in young rats. The parameters observed were: urea, glycemia, hepatic glycogen, blood and kidney d -aminolevulinate dehydratase (d -ALA-D) activities and changes in body weight gain. Wistar rats with 30 days old were intraperitoneally injected with saline or alloxan 150 mg/kg after 24 hour fasting. After 2 weeks, a 2^nd dose of saline or alloxan (125 mg/kg) was administered after 24 hour fasting. At 20, 40 or 60 days from last dose the animals were weighed and killed (after 12 h fasting). Liver and kidneys were taken out and blood colleted using heparinized syringe. We observed that at 20 days from last dose, the rats presented glycemia equal to control. At 40 and 60 days after injection of alloxan, only 50 and 13% of alloxan injected rats presented a significant increase of glycemia. These hyperglycemic animals (both at 40 and 60 days after alloxan) presented significant alterations on almost all parameters analyzed (control x hyperglycemic alloxan rats, respectively): lower weight gain (40 days: 313 x 211 g; 60 days: 304 x 255 g), increase of glycemia (40 days: 112.7 x 269.6 mg/dL; 60 days: 89.2 x 264.8 mg/dL), urea (40 days: 40.0 x 118.1 mg/dL; 60 days: 37.5 x 96.0 mg/dL) and glycogen (40 days: 0.8 x 4.2 g%; 60 days: 1.0 x 3.1 g%). The d -ALA-D activity was not altered in neither of the intervals analyzed. The hyperglycemia and high urea levels presented by alloxan rats are according to other studies that have used alloxan as diabetogenic inductor. This model is characterized for hyperglycemia due to the destruction of pancreatic b -cells, and high uremia due to a small utilization of carbohydrates and consequent increase protein degradation. These features can be responsible for high glycogen levels presented for diabetic rats. The absence of the effect on kidney and blood d -ALA-D activities can be due to drug used to induce diabetes, since the decrease in this enzyme activity was obtained in rats submitted to diabetes using streptozotocin.