![]() ![]() These observations urge for the need of animal models to study the mechanistic link between vitamin D deficiency and these clinical conditions. ![]() Clearly, adequate strategies for vitamin D supplementation could help attenuate the incidence of these disorders, as suggested by the recent meta-analysis on the efficacy of cholecalciferol (vitamin D 3), but not ergocalciferol (vitamin D 2), supplementation in reducing mortality rates. In fact, vitamin D deficiency associates with an increased risk of hypertension, cardiovascular disease, infectious and autoimmune diseases, glucose intolerance, albuminuria, and cancer. The epidemiological association between vitamin D deficiency and high mortality rates extends beyond the abnormal mineral homeostasis that impairs bone mineralization due to high serum levels of PTH. The high incidence of obesity in the US population is an additional determinant of vitamin D deficiency, as circulating levels are lower due to dilution in the fat mass. Racial factors include a darker skin pigmentation, which limits conversion rates in spite of similar exposure to sun light. Cultural factors that limit skin exposure to sun light are clothing, age, sex, and the use of sunscreen protectors. However, the high prevalence of vitamin D deficiency in the otherwise healthy US population varies not only depending upon seasonal changes, but also depending on cultural and racial factors. Due to the small content of vitamin D in nonsupplemented food, circulating vitamin D levels are mainly determined by the amount of sunlight exposure. In the US adult population, 42% is vitamin D deficient (25D serum levels <50 nmol/L <20 ng/mL). Vitamin D deficiency is a worldwide problem as it associates with increased mortality for all causes. Therefore, this model provides a useful tool to examine the sole effect of hypovitaminosis D, in a wide range of research settings, without confounding changes in PTH, Ca, and P. After three weeks, serum 25-hydroxyvitamin D 3 (25D) and 1,25-dihydroxyvitamin D 3 (1,25D) levels had dropped below detection limits, with unchanged serum PTH, Ca, and phosphate (P) levels. Secondly, six intraperitoneal injections of paricalcitol during the first two weeks are given to induce the rapid degradation of circulating vitamin D metabolites. Firstly, the vitamin D depleted diet is calcium (Ca) enriched, to attenuate the development of secondary hyperparathyroidism. We incorporated two additional manoeuvres compared to a conventional diet. ![]() To overcome these shortcomings, we report the successful induction of vitamin D deficiency within three weeks, with stable serum PTH and minerals levels, in Wistar rats. More importantly, induction of hypovitaminosis D causes significant fluctuations in parathyroid hormone (PTH) and mineral levels, complicating the interpretation of study results. Current vitamin D deficient rat models have important practical limitations, including time requirements when using, exclusively, a vitamin D deficient diet. To study the mechanisms involved and improve treatments, animal models are tremendously useful. ![]() Vitamin D deficiency is associated with a range of clinical disorders. ![]()
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