The Nicotinamide/Streptozotocin Rodent Model of Type 2 Diabetes: Renal Pathophysiology and Redox Imbalance Features

Diabetic nephropathy (DN) is a common complication of diabetes mellitus. While there has been a great advance in our understanding of the pathogenesis of DN, no effective managements of this chronic kidney disease are currently available. Therefore, continuing to elucidate the underlying biochemical and molecular mechanisms of DN remains a constant need. In this regard, animal models of diabetes are indispensable tools. This review article highlights a widely used rodent model of non-obese type 2 diabetes induced by nicotinamide (NA) and streptozotocin (STZ). The mechanism underlying diabetes induction by combining the two chemicals involves blunting the toxic effect of STZ by NA so that only a percentage of 13 cells are destroyed and the remaining viable 13 cells can still respond to glucose stimulation. This NA-STZ animal model, as a platform for the testing of numerous antidiabetic and renoprotective materials, is also discussed. In comparison with other type 2 diabetic animal models, such as high-fat-diet/STZ models and genetically engineered rodent models, the NA-STZ model is non-obese and is less time-consuming and less expensive to create. Given that this unique model mimics certain pathological features of human DN, this model should continue to find its applications in the field of diabetes research.

Automated summary

Diabetic nephropathy (DN) is a common complication of diabetes mellitus, and there are currently no effective treatments available. Understanding the biochemical and molecular mechanisms of DN requires the use of animal models, and one widely used model is the non-obese type 2 diabetes induced by nicotinamide and streptozotocin in rodents.