Document Detail


Enhanced excretion of vitamin D binding protein in type 1 diabetes: a role in vitamin D deficiency?
MedLine Citation:
PMID:  20943786     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
CONTEXT: Vitamin D deficiency is an increasingly recognized comorbidity in patients with both type 1 (T1D) and type 2 diabetes, particularly associated with the presence of diabetic nephropathy.
OBJECTIVE: Because we have previously reported enhanced excretion of megalin in the urine of T1D patients with microalbuminuria, we hypothesized that concurrent urinary loss of the megalin ligand, vitamin D binding protein, might contribute mechanistically to vitamin D deficiency.
DESIGN AND PARTICIPANTS: Examining a study cohort of 115 subjects with T1D, aged 14-40 yr, along with 55 age-matched healthy control subjects, we measured plasma and urine concentrations of vitamin D binding protein (VDBP) along with serum concentrations of total calcium, parathyroid hormone, 25-hydroxyvitamin D, and 1, 25-dihydroxyvitamin D; these results were compared between groups and investigated for relationships with metabolic control status or with albuminuria.
MAIN OUTCOME MEASURE: Between-group differences in urinary VDBP concentration were the main outcome measures.
RESULTS: A marked increase in the urinary excretion of VDBP was apparent in subjects with T1D, compared with control subjects. Using multivariate regression modeling, significant correlates of urinary VDBP excretion included microalbuminuria (P = 0.004), glycosylated hemoglobin (P = 0.010), continuous glucose monitoring system average capillary glucose (P = 0.047), and serum 1,25(OH)(2)D concentrations (P = 0.037). Vitamin D deficiency or insufficiency was slightly more prevalent in diabetic subjects with albuminuria, coincident with the increase in urine VDBP excretion.
CONCLUSIONS: These findings suggest that, theoretically, exaggerated urinary loss of VDBP in T1D, particularly in persons with albuminuria, could contribute mechanistically to vitamin D deficiency in this disease.
Authors:
Kathryn M Thrailkill; Chan-Hee Jo; Gael E Cockrell; Cynthia S Moreau; John L Fowlkes
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-10-13
Journal Detail:
Title:  The Journal of clinical endocrinology and metabolism     Volume:  96     ISSN:  1945-7197     ISO Abbreviation:  J. Clin. Endocrinol. Metab.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2011-01-06     Completed Date:  2011-02-04     Revised Date:  2012-01-02    
Medline Journal Info:
Nlm Unique ID:  0375362     Medline TA:  J Clin Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  142-9     Citation Subset:  AIM; IM    
Affiliation:
Department of Pediatrics, Arkansas Children's Hospital, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72202, USA. thrailkillkathrynm@uams.edu
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MeSH Terms
Descriptor/Qualifier:
Adolescent
Adult
Blood Glucose / metabolism
Calcium / blood
Diabetes Mellitus, Type 1 / complications,  metabolism*
Female
Humans
Male
Parathyroid Hormone / blood
Regression Analysis
Vitamin D / analogs & derivatives,  blood
Vitamin D Deficiency / complications,  metabolism*
Vitamin D-Binding Protein / metabolism*
Grant Support
ID/Acronym/Agency:
C06RR16517/RR/NCRR NIH HHS; M01 RR14288/RR/NCRR NIH HHS; R01-DK62999/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/Parathyroid Hormone; 0/Vitamin D-Binding Protein; 1406-16-2/Vitamin D; 64719-49-9/25-hydroxyvitamin D; 66772-14-3/1,25-dihydroxyvitamin D; 7440-70-2/Calcium

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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