Peculiar glycemic patterns in alloxan-induced diabetes animal model

Abstract

Animals are commonly used for experimentation in academic and research institutions (Kimwele et al, 2011). The reliability of a study is partly determined by the animal model used. The researcher must therefore have a fine understanding of animal models when designing animal studies. The current study focuses on animal models used in investigating diabetes mellitus (DM) and its management. These animal models differ significantly, and no single one has been reported to accurately represent the essential pattern of type 2 DM in humans, in whom the disease is often preceded by obesity and various molecular changes. Animal models are developed by techniques such as pancreatectomy, chemical induction, genetic engineering, molecular biology, and islet cell transplantation (Junod et al, 1969). They are conducted in animal models, notably dogs and rodents (Lanza et al, 1999).

In the majority of studies, chemical-induced diabetes models have been utilized (Frode and Medeiros, 2008). Such chemicals include alloxan (Lenzen, 2008) and streptozotocin (Junod et al, 1969). As of 2010, streptozotocin had reportedly been used in 69% of chemical-induced diabetes animal models, whereas alloxan was the second most commonly used chemical at 31% (Etuk, 2010).

Alloxan is a urea derivative that causes selective necrosis of the pancreatic islet β-cells (Etuk, 2010). It is used experimentally to induce type 2 DM in animals such as rabbits, rats, mice, and dogs. The experimental dose of the drug needs careful consideration to avoid excessive pancreatic tissue damage. The most frequently used intravenous dose of alloxan in rats is 65 mg/kg, but its effective dose must be higher when it is administered intraperitoneally or subcutaneously (Antia et al, 2005). With the rising use of alloxan-induced DM models, different dosages and different methods of inducing diabetes have been reported. Though most methods have demonstrated success, a handful have reported failed induction or variation in blood glucose following alloxan administration (Etuk, 2010). The current study was thus carried out to assess the pattern of blood glucose following intraperitoneal administration of alloxan (125 mg/kg).