Whole Egg consumption attenuates vitamin D insufficiency in type 1 diabetic rats
Authors: Saande Cassondra J. , Schalinske Kevin L. , Rowling Matthew J. 
Published: November 2023

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.

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