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Vitamin D homeostasis is disrupted in a type II diabetic rat model due to aberrant reuptake in kidney
Author(s) -
Anderson Rachel Lynn,
Rowling Matthew J
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.325.6
Subject(s) - medicine , endocrinology , vitamin d and neurology , reabsorption , diabetes mellitus , homeostasis , vitamin , kidney , type 2 diabetes , hormone
Alterations of serum levels of the major circulating form of vitamin D (25‐hydroxycholecalciferol, 25D 3 ) and its active hormone derivative (1,25‐dihydroxycholecalciferol, 1,25D 3 ) have been associated with type II diabetes, but a mechanism for this occurrence has not been fully elucidated. In this study, we used the Zucker Diabetic Fatty (ZDF) rat model to characterize the role of renal reabsorption in vitamin D homeostasis in diabetic and non‐diabetic rats fed vitamin D sufficient (1000 IUs/kg), deficient (0 IUs/kg), and supplemented diets (10000 IUs/kg). Using ELISA, we analyzed serum and urinary 25D 3 , 1,25D3 and vitamin D binding protein (DBP) levels in 16 wk old ZDF and lean rats. Serum levels of both 25D 3 and 1,25D 3 were significantly lower in diabetic animals than their non‐diabetic controls fed either vitamin D deficient or sufficient diets. Furthermore, diabetic rats excreted greater proportions of DBP and 25D 3 in urine than their respective controls. Vitamin D supplementation markedly increased serum 25D 3 in diabetic rats, but had no effect on serum 1,25D 3 or urinary excretion ratios. Taken together, these data suggest that compromised renal reabsorption of 25D 3 and DBP may be a significant contributing mechanism leading to reduced vitamin D status in diabetes. Supported by USDA (Iowa State University Nutrition and Wellness Center SRPG to MR) and the Iowa State University Experiment Station.