A REVIEW OF METHODS FOR INDUCING VITAMIN B12 DEFICIENCY IN ANIMAL MODELS

Abstract

Vitamin B12 (cobalamin) deficiency is a significant global health issue, particularly impacting older adults, vegetarians, and those with gastrointestinal disorders. It is linked with a broad spectrum of clinical symptoms, including megaloblastic anaemia, neurological impairments, and cardiovascular problems. To explore the pathophysiology of this deficiency and assess potential therapeutic approaches, animal models are essential. This review concentrates on various established techniques for inducing vitamin B12 deficiency in animal models, particularly rodents. Three main methods are examined: the nitrous oxide-induced functional deficiency model, the restricted diet model, and the modified diet model that omits vitamin B12. The nitrous oxide model is swift and can reproduce the neurological and hematologic symptoms of deficiency; however, it carries risks such as hypoxia and neurotoxicity. The restricted diet model consists of feeding animals a diet devoid of B12 for a prolonged period, which is safer but requires more time. The modified diet model incorporates pectin, which binds to intrinsic factor and obstructs B12 absorption, providing an alternative way to mimic issues with bioavailability. Each method presents unique advantages and drawbacks regarding safety, induction duration, reproducibility, and clinical relevance. Additionally, this review outlines the physiological pathways for B12 absorption and emphasizes the diagnostic tools utilized to evaluate deficiency, including serum B12 levels, methylmalonic acid, homocysteine, and holotranscobalamin. Gaining insight into these models and diagnostic methods is crucial for progressing research on vitamin B12 deficiency and crafting more effective prevention and treatment options. This review acts as a guide for researchers in choosing suitable models to investigate the clinical and biochemical dimensions of vitamin B12 deficiency.