Vitamin D homeostasis is compromised due to increased urinary excretion of the 25-hydroxycholecalciferol-vitamin D-binding protein complex in the Zucker diabetic fatty rat
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Abstract
Maintaining optimal vitamin D status is known to be a protective factor in many diseases. Furthermore, altered vitamin D status is often associated with non-insulin dependent diabetes mellitus (NIDDM), although the reason for this association remains unclear. Since impaired renal reabsorption of circulating vitamin D and its carrier protein has been shown to lead vitamin D deficiency, we hypothesized that renal proteins involved in vitamin D reabsorption may be reduced in NIDDM, thus contributing to compromised vitamin D homeostasis. We used the Zucker diabetic fatty rat model of NIDDM to examine urinary excretion of vitamin D metabolites and renal proteins involved with reabsorption of protein-bound vitamin D. We found that vitamin D status was impaired and indications that renal reuptake of protein-bound vitamin D was reduced in NIDDM rats compared controls. Our findings suggest that reduced renal vitamin D reabsorption may contribute to compromised vitamin D status in NIDDM.