Type 1 diabetes (T1D) is characterized by vitamin D insufficiency due to increased urinary excretion of 25-OH-vitamin D (25D) and its circulatory transporter vitamin D binding protein (DBP). Whole eggs are a significant dietary source of 25D, the major circulating form that is an index of vitamin D status and the precursor for active 1,25-(OH)2-vitamin D. Thus, we hypothesized that dietary consumption of whole egg represents an effective dietary strategy to maintain vitamin D balance in T1D. To address our hypothesis, we assessed whether feeding a whole egg-based diet would attenuate or prevent compromised vitamin D homeostasis using a streptozotocin (STZ)-treated Sprague-Dawley rat as a model of T1D. T1D rats (n=12) were randomly assigned to either a control AIN93 casein-based diet or a whole egg-based diet, both provided at 20% (w/w) of the diet with respect to protein content. Control rats (n=6) received the casein-based diet. Both the casein-based and whole egg-based diets contained the same total lipid content (16.3%, w/w) by the addition of corn oil to the casein-based diet to match the lipid contribution by the addition of whole egg. After 25 days of consuming the whole egg- or casein-based diets, T1D rats received a single intraperitoneal injection of STZ in citrate buffer (10 mM, pH 4.5); control rats were vehicle-injected. All rats were sacrificed 7 days after STZ or vehicle injection. Rats were placed in metabolism cages 12 hours prior to sacrifice for the collection of urine and to ensure they were in a fasted state. Mean values from all of the analyses were compared using a one-way ANOVA (one-tailed, P<0.05). Body weights did not differ between groups prior to STZ or vehicle injection. As expected, the administration of STZ resulted in a decrease in body weight in both T1D groups; T1D rats fed the casein-and whole egg –based diets exhibited an 8 and 11% decrease in body weight, respectively, compared to their body weights prior to induction of diabetes. Serum 25D concentrations of T1D rats fed the whole egg-based diet were increased 80 and 67% compared to control and T1D rats fed the casein-based diet, respectively. Urinary concentrations of 25D were elevated 4-fold in T1D rats fed the casein-based diet compared to control rats fed the casein-based diet. However, urinary 25D concentrations did not differ between T1D rats fed the whole egg-based diet and control rats fed the casein-based diet. Similarly, T1D rats fed the casein-based diet exhibited urinary concentrations of DBP that were 17-fold higher than non-diabetic controls and DBP concentrations of T1D rats fed the whole egg-based diet did not statistically differ from control values. Likewise, total urinary protein was increased 5-fold in T1D rats fed the casein-based diet compared to controls, whereas total urinary protein did not differ between the T1D rats fed the whole egg –based diet as compared to control rats fed the casein-based diet. These data demonstrate that a whole egg-based diet can increase serum 25D concentrations and diminish diabetic nephropathy, thereby preventing urinary excretion of 25D. Our studies support the concept that a whole egg-based diet may be a viable dietary strategy to maintain vitamin D homeostasis in type 1 diabetes.
