Combined Administration of Streptozotocin and Sucrose Accelerates the Appearance of Type 2 Diabetes Symptoms in Rats

Abstract

Type 2 diabetes is a disease with a high global prevalence, characterized by chronic hyperglycemia, insulin resistance, polyphagia, polydipsia, polyuria, and changes in body weight. Animal models have been very useful for the study of this disease and to search for new therapeutic targets that delay, attenuate, or avoid diabetic complications. The purpose of this work was to establish a model of type 2 diabetes and exhibit the majority of the characteristics of the disease. Two-day-old male and female Wistar rats were treated once with streptozotocin (70 or 90 mg/kg body weight). After weaning, they were given a sucrose-sweetened beverage (SSB; sucrose at 10 or 30%) during 7 or 11 weeks; their body weight and food intake were measured daily. With the rats at 14 weeks of age, we determined the following: (a) fasting blood glucose, (b) oral glucose tolerance, and (c) insulin tolerance. We found that the supplementation of sucrose at 10% for 7 weeks in male rats which had previously been given streptozotocin (70 mg/kg) at neonatal stage leads to the appearance of the signs and symptoms of the characteristic of type 2 diabetes in adulthood.

Figure 1

Experimental scheme of diabetes induction in Wistar rats. Two-day-old male and female rats were injected with STZ (70 or 90 mg/kg) intraperitoneally (i.p.). The rats were immediately returned to their mothers and weaned at 21 days of age. In addition, rat groups with and without 70 mg of STZ/kg body weight were supplemented with SSB (standard commercial sucrose) at 10% or 30% for either 7 or 11 weeks after weaning. The Control group was included that was not exposed to STZ nor to SSB. Body weight and food intake were monitored daily for 6 weeks (when the rats were 8-14 weeks of age), and fasting blood glucose was measured at weeks 10 and 14 of age. Afterward, the insulin tolerance test (ITT) and glucose tolerance test (GTT) were performed at week 14.