This technology provides a method for creating a diabetic animal model by applying chronic immobilization stress—restricting the movement of laboratory animals for a set time daily for several weeks—and administering streptozotocin midway to selectively damage pancreatic beta cells. This model exhibits increased blood nitric oxide levels, reduced endothelium-dependent relaxation, and decreased heart rate.
Diabetes causes endothelial dysfunction and cardiovascular complications due to the accumulation of reactive oxygen species and excessive nitric oxide from persistent hyperglycemia. Existing Type 2 diabetes animal models have limitations: genetic models are costly, high-fat diet models take a long time to induce diabetes, and pancreatectomy models are technically demanding. Furthermore, although stress is a major risk factor for Type 2 diabetes, no animal models have previously incorporated stress conditions.
This technology induces diabetes physiologically without genetic modification using simple stress induction—such as restraining animals with towels, plastic boxes, PVC pipes, or metal cylinders—combined with drug administration. It mimics the high serum nitric oxide levels seen in clinical Type 2 diabetes patients. The shortened induction period reduces experimental costs, and the model can be used to study vascular diseases related to diabetes and hypertension, such as atherosclerosis, myocardial infarction, and stroke. It is applicable for preclinical efficacy testing of new drugs for diabetic vascular complications, research into stress-related metabolic disease mechanisms, and validation of vascular-protective materials, enabling low-cost, rapid testing of diabetic complications that reflect modern chronic stress environments.
This invention was developed with support from the Ministry of Education for research into the mechanisms of natural products in controlling hypoxic cerebrovascular damage.
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